Larynx: (Vagus) Pulmonary Lung Compliance Chest Wall ComplianCO has a 200-250 X greater affinity for HgB than O2

Motor: External Superior Laryngeal = Cricothyroid Peds ↓  (d/t  ↓  #  alveoli) ↑

(stim of SLN = laryngospasm) Geri ↑ ↓
Recurrent Laryngeal = everything else 4 ways CO2 is carried in Blood:
Sensory: Internal Superior Laryngeal = Above Vocal Cords & Cords V/Q Alveolar V/Q = 4/5 = 0.8 [MV/CO] 1. Physically dissolved (5%)
Recurrent Laryngeal = Below Vocal cords PaO2 size V/Q = 10/0 = ∞ = dead space 2. Carbonic Acid (<1%)
Posterior Cricoarytenoid = Abduct PCO2 V V/Q = 0/10 = 0 = shunt 3. Bicarbonate Ion (HCO3-, 90%)
“You  take  it  out  back” Q 4. Protein Bound (5%)
Lateral Cricoarytenoid = Adduct
“You  bring  it  in  from  the  side” CO2 is 20 X more soluble than O2
Cricothyroid = Tenses vocal cords Intrapleural pressure (-) usually / + w/ Valsalva and forced expiration CO2 produced/min = 200 ml/min or 2.4-3.2 ml/kg/min
Thyroarytenoid = Relaxes cords Intrapulmonary (-) inspiration (+) expiration
Dissolved: O2 = 0.003 x _______ CO2= 0.067 x _______
Pharynx: Physiologic Dead Space = Anatomic DS + Alveolar DS
Motor: Spinal Accessory Anatomic DS = Conducting air passageways + ETT 2ml/kg Total CO2 content of arterial blood = 48 ml CO2/100 ml blood
Sensory: Glossopharyngeal Alveolar DS = Ventilation without perfusion Total CO2 content of venous blood = 52 ml CO2/100 ml blood
Laryngeal Cartilages Alveolar ventilation = (TV –DS) x RR
Epiglottis Superior Dead Space = well vent/poor perfusion Shunt= well perfuse/poor vent Normal CO2 arterial-venous difference = 4 ml CO2/100 ml blood
Thyroid ↑Dead Space 1. Age, 2. PP Vent 3. PE 4. Lung Dz
Cuneiform (P) Minute ventilation = TV x RR Carbonic Anhydrase is responsible for converting CO2 to HCO3-
Corniculate (P)
Arytenoids (P) Compliance = V/ P Central chemoreceptors respond to H+ in the CSF
Cricoid Inferior Un-anesthetized Anesthetized Peripheral chemoreceptors respond to H+, CO , and PaO
2 2
Lateral Decubitus V Q V Q
Oxyhemoglobin Dissociation Curve Non-dependent PaCO2 is the primary stimulus for ventilatory response
Dependent
Mast cells can cause bronchoconstriction through histamine
Percent Jackson-Reese: minimum flow = 5 L/min (2.5-3 X MV) release.
Hemoglobin (Modified Mapleson E)
Saturation Bain Circuit min. flow = 70 ml/kg for CV, or 100-300 ml/kg for 6 anatomical characteristics of a difficult intubation:
SV (Modified Mapleson D) [Link], muscular neck 2. Receding mandible
PaO2 = FiO2 X 5 PaO2 = 102 –Age/3 on RA 3. protruding maxillary incisors 4. Unable 2 visualize uvula
PAO2 = FiO2 X 6 PaO2=100 –(0.4 x age) 5. limited tempromandibular joint <40mm
P50 PAO2-PaO2 = (40 X 6) – (40 X 5); if FiO2 = 40% 6. Limited cervical mobility
CPAP = nondependent (up) Normal A-aO2 = 5-15 mm Hg on RA
Blood PO2 PEEP = dependent (down) 5 Contraindications to FOB
Normal P50 = 26-27 mm Hg
[Link] 2. Heave airway secretions
Left Shift Right Shift 3. bleeding not relieved w/ suction 6. LA allergy
IRV IC 5. inability to cooperate
PCO 2 PCO 2
H+ H+
COPD:
pH pH TV VC TLC* The permanent dilation of a bronchus or group of small bronchi,
Temp Temp airway resistance increases, compliance increases
CO poisoning 2-3 DPG 1. Large tidal volume (10-15 ml/kg)
(Carboxyhemoglobin) Sickle Cell FRC* ERV CV 2. Slow inspiratory flow rate
Fetal hemoglobin Closing 3. Slow respiratory rate
Methemoglobin (Prilocaine, Nitroprusside) RV* Capacity Bronchitis:  copious  sputum,  ↑Hct,  “Blue  Bloater”
Smoking Emphysema:  cough  w/  exertion,  scant  sputum,  “Pink  Puffer”
*cannot be directly measured through spirometry Post op ventilation: FEV1/FVC <.50 & Preop CO2 >50mmHg
Right shift unloads O2 from blood, Right = Released PFT’s
Left shift increases O2 affinity - Left = Locked Obstructive: COPD (hard to get out) Normal Asthma
Asthma, Bronchitis, Emphysema FEV1 = 4 L Wheezing #1
“Bohr  effect”  PaCO2 affects Oxyhemoglobin dissociation curve FEV1 2.5 L FVC = 5 L Hypoxia & Hypocarbia w/ alkalosis
“Haldane  effect”  PaO2 affects CO2 dissociation curve FVC = normal FEV1/FVC = 0.8
“Hamburger  shift”  Cl- exchange for HCO3- in  RBC’s: FEV1/FVC (low) = 0.7 FEV25-75 = 4.7 L/sec Two most common Reasons for Pulmonary Edema:
HCO3- out, Cl- in; non-pulmonary FEV25-75 is the best test to assess early stages of COPD-small in Pulmonary hydrostatic pressure
airway dz in permeability of alveolar-capillary membrane
SaO2 PaO2 Restrictive: (hard to get in) Colloid osmotic pressure = 28 mmHg
90% 60mmHg Pulmonary fibrosis, Pneumothorax, Scoliosis Hydrostatic pressure = 6-8 mmHg
70% 40mmHg FEV1
FVC Causes of ARDS: Right to Left Shunt
Dissolved O2 = 0.003 X PaO2 FEV1/FVC = normal to high 1. Shock
O2 bound to HgB = (1.34 X HgB) (SaO2) Moderate risk: If FEV1 2 L & FEV1/FVC 50% then more 2. Fat or air embolism
Total O2 Content = (0.003 X PaO2) + (1.34 X HgB) (SaO2) tests, e.g. split-lung function tests. (i.e do not proceed) 3. Aspiration
O2 Consumption 250 ml/min 3-4 ml/kg/min High Risk: FEV1<1, FVC <1.5L or 20m/kg FEV1/FVC < 35% 4. Burns
Dissolved CO2 = 0.067 X PaCO2 5. Sepsis
CO2 produced & eliminated @ 200ml/min Flow Volume Loops: 6. Trauma
7. Drug ingestion
Obstructive = baby carriage
Control of Ventilation: (brainstem) 8. Uremia
Restrictive = small normal 9. Pancreatitis
Primary Respiratory Centers:
10. Massive blood transfusion
Dorsal Respiratory Group (DRG) Pacemaker
11. Head injury
~phrenic & external intercostals Medulla 12. Cardiopulmonary bypass
Ventral Respiratory Group 13. Radiation of thorax
~internal intercostal Obstructive Restrictive 14. Drowning
Hypoxia is the #1 manifestation of ARDS
Secondary Respiratory Centers:
Apneustic Center Normal Five types of Hypoxia:
~ deep & prolonged respiration Pons 1. Hypoxic hypoxia (diffusional)
Pneumotaxic Center 2. Anemic hypoxia (↓Hbg concentration)
~Shuts off respiration (Hering-Bering 1.5L) Intrathoracic 3. 20 venous to arterial cardiac shunts
Obstruction Extrathoracic 4. Histotoxic hypoxia (cyanide poisoning #1, toxicity, vitamin
Neuro: Central Chemoreceptors in medulla H+ -PCO2 in CSF poisoning)
Obstruction
5. Hypoxia 20 pulmonary disease
Peripheral Chemoreceptors: O2 < 60 mmHg
Carotid: Glossopharyngeal CO2 ↓expiration Fixed
S/S of Aspiration: ( risk: pH < 2.5, gastric volume > 25 ml)
Aortic: Vagus (Afferent) H+ ↓inspiration obstuct
(Mendelson’s  syndrome)
Stretch Receptors: Vagus 1. Wheezing
Alveolar ventilation = Minute Ventilation – Dead Space Ventil. 2. Coughing
Partial Pressure of CO2 in CSF = LeChatelier’s Principle 3. Cyanosis
Hyperbaric O2 used to treat: 4. Pulmonary edema
Hering-Breuer reflex: Vagus nerve, prevents over-stretching (TV 1.5L) 1. CO2 poisoning 5. Shock
2. Gas embolism 6. Hypoxemia- earliest & most reliable sign
Inspiration  =  ↑  HR d/t  ↓  intrathoracic  pressure 3. Anaerobic infections (gas gangrene) ARDS most serious complication
4. Decompression sickness (Bends)
Four causes of Pulmonary Restrictive Disease: Stress (exercise) ECG has 90% specificity (rules in CAD). Arterial Line:
1. Acute intrinsic restrictive lung disease (ARDS, aspiration, or CHF)
2. Chronic intrinsic restrictive lung disease (sarcoidosis, drug-induce) Autoregulation: 3
3. Chronic extrinsic restrictive lung disease (obesity, ascites, pregna.) “big   Cerebral Perfusion Pressure = MAP 50-150 mmHg 1
bellies” Coronary Perfusion Pressure = MAP 60-160 mmHg 2
4. Disorders of the pleura or mediastinum
Renal Perfusion Pressure = MAP 80-180 mmHg
1 = anacrotic limb: contractility & SVR(ease of LV emptying)
Sarcoidosis
Intrinsic restrictive lung disease Goldman Cardiac Risk Index: (most significant) 2 = dicrotic limb: blood flow to periphery
Restrictive  ♥  myopathy Recent MI 3 = dicrotic notch: aortic valve closure, coronary artery perfusion
↑  Ca++ S3 Gallop (CHF) Pulse  pressure  greatest  in  pedis  d/t  ↑SBP  &  ↓DBP
Splenomegaly High transducer = Low BP Low transducer = High BP
Hepatic granulomas Four types of abnormal Cardiac wall motion: Invasive BP is 20 mmHg higher than non-invasice
Optic and facial nerve involvement 1. Hypokinesis (less than normal wall motion) Sitting position = transducer @ ear
2. Hyperkinesia (greater than normal wall motion)
S/S of tension pneumothorax: 3. Akinesis (absence of wall motion) 1 Vent. Action Potential
Hypotension 4. Dyskinesis (paradoxical outward motion) 2 0 = Na+ influx
+ +
Hypoxemia (Na influx) 0 3 (K out) 1 = Cl- in, K+ out
Tachycardia 2 = Ca++ influx
CVP QRS 4 3 = K+ efflux
PIP 4 = Na+-K+ pump
Absence of unilateral breath sounds
Tracheal shift S-A Node Act. Potential
Asymmetric chest wall movement a c v (Ca++ influx) 0 3 0 = Ca++ influx
threshold and Na+ (mostly
Transtracheal Jet Vent: CVP Ca++)
Cricothyroid membrane x y 0-11mmHg
4 4
Complications of Transtracheal Jet Ventilation: SV = CO/HR 60-90 ml/min
Barotrauma & pneumothorax Sub Q emphysema Systole CI = CO/BSA 2.5-3.5 L/m/
Mediastinal air (emphysema) Exhalation difficulty SI = CI/HR 40-60
Arterial perforation Esophageal puncture a = atrial contraction SVR = 80(MAP-CVP/CO) 900-1500 dyn
Damage to tracheal mucosa Thickened secretions c = ventricular contraction, tricuspid valve elevation PVR = 80(MPAP-PCWP/CO) 50-150 dynes
v = tricuspid closed, systolic atrial filling CoPP =AoDBP-PCWP 60-160 mmHg
Ventilation modes x= vent systole, atrial relax, displace tricuspid valve MAP = DBP + 1/3(SBP-DBP) 80-120 mmHg
spontaneous ventilation : IMV, SIMV, MMV, PSV & HFJV y=diastole, early vent filling, open tricuspid
Do not support spont vent: CMV, AC, and PCV RBBB: V1 =  rsR’,  broad  R  wave
RIJ preferred – LIJ has the thoracic duct V6 = qRS, broad S wave
Respiratory medications LBBB: V1 = no R wave, wide negative S wave
Aminophylline is a phosphodiesterase inhibitor (PDEIII). Large A waves: tricuspid stenosis, pulmonary stenosis, V6 = no Q wave, wide notched R wave
Phosphodiesterase breaks down cAMP. When phosphodiesterase is pulmonary  HTN,  ↓  right  ventricular  compliance
inhibited, cAMP accumulates and bronchodilation occurs. It also Inferior, Posterior II, III, aVF RCA
improves diaphragmatic contractility. Xanthines cause release of NE Large V waves: tricuspid regurg, r vent papillary muscle Lateral I, aVL, V5-V6 Left Circumflex
from sym postganglionic neurons – avoid w/ halothane, adenosine ischemia, pericarditis, cardiac tamponade Anterior, Septal V1-V4 LAD
receptors
Multiorifice catheter = 2cm below SVC Dsyrthmias with MI:
Caffeine and Theophylline are both methylated xanthines. Single orifice catheter = 3cm above SVC Inferior or posterior: Obstruction of the RCA or circumflex = SA
T4-T5 interspace above level of 3rd rib & AV nodal dysrhythmias -sinus arrest, sinus pause, type I AV
Beta-2 receptor stimulation activates adenylate cyclase which block, nodal rhythms, & complete heart
converts ATP to cAMP resulting in bronchodilation. Increased CVP:
Right ventricular failure, tamponade, tricuspid stenosis, tricuspid Anterior MI: Wide complex rhythms- bundle branch block,
Cromolyn sodium is a mast cell stabilizer that prevents the release of regurgitation, pericarditis, pulmonary hypertension, chronic left complete heart block, mobitz type II block, idioventricular
histamine, bradykinin. It prevents bronchospasm in asthmatics, but is ventricular failure, and hypervolemia rhythms.
not effective once bronchospasm develops. CHRONIC
PEEP may read high- need to d/c from vent 10-15 seconds ECG electrodes: 1 millivolt or 1000 microvolts
Ipratroprium, a quaternary ammonium compound, is an
antimuscarinic used to augment bronchodilation produced by beta-2 Venous baroreceptors: Modified V5 lead
agonists. Blockade of the muscarinic receptor leads to a decrease of RA & great veins Bainbridge reflex, stretch of Right Atrium place the LL and RA leads in normal positions, then place the LA
IP3 so less calcium is released form intracellular vesicles. Smooth = Increases HR with inspiration via vagus nerve. lead over the anterior axillary line at the level of 5th intercostal
muscle tone is reduced. space & select Lead I as the monitoring lead.
Arterial baroreceptors:
Doxapram is a non-xanthine central respiratory stimulant. It increases Aortic arch Vagus nerve afferent, stretch U wave
tidal volume and to a lesser extent respiratory rate. It is not good for Carotid sinus Glossopharyngeal  (Hering’s)  nerve  afferent small positive wave following T wave.
newborns because it is dissolved in benzyl alcohol. It acts through Action potentials (efferent) via vagus and T1-T4 sympathetic associated w/  ↓  K, ↑  Ca, quinidine, digitalis, epinephrine,
peripheral chemoreceptors to stimulate central chemoreceptors. cardio accelerators. intracranial hemorrhage, or papillary muscle dysfunction

ETT = Age/4 + 4 (uncuffed) Length = 12 + Age/2 Swan-ganz Catheters: (1.5ml – max balloon) LV Pressure Volume Loop:
(-) 0.5 cuffed Normal pressures & depth of insertion from R IJ Aortic valve closes ejection
mm Hg Depth in cm RIJ +10 RV + 15 PA Systole endsD
Wt in Kg LMA Cuff vol ETT FOB RA 1-8 20 30 45 Left C Aortic valve opens
6.5 1 4 cc 3.5 2.7 RV 15-25/1-8 30 Ventricular
20 2 10 4.5 3.5 PA 15-25/8-15 45 Pressure SV
Isovolumic Isovolumic
20-30 2.5 14 5.0 4.0 PCWP 6-12 45-50 Relaxation Contraction
30 3 20 6.0 5.0 LA 2-12
nor adult 4 30 6.0 5.0 LV 100-140/0-12
lrg adult 5 40 7.0 5.0 B
lrg adult 6 50 7.0 5.0 PAWP is NEVER higher than PADP A Mitral valve closes
In  can  be  in:  MS,  ↑  alveolar  pressure,  pulmonary  venous  obstruc Mitral valve opens Systole Starts
*Size is based on weight! Left Ventricular Volume
Patient Status CVP PCWP
Sterilization temperatures: 275F & 135C Hypovolemia Low Low Preload = SV, same ED vol = (Give fluids)
Regurg: head down (#1), disconnect circuit, sx, examine w/ Left vent failure Normal or High High Preload = SV, same ED vol = (NTG, Lasix, tamponade)
bronchoscope, x-ray, abx (debatable), physiotherapy Right vent failure High Normal Afterload = SVR, SV, BP, ED vol = (phenylephrine)
Cleaner: Endozime PE High Normal Afterload = SVR, SV, BP, ED vol = (SNP)
Chronic Pulm Htn High Normal Contractility = SV, ED vol, BP = (Digoxin, Ca++)
Differences in Neonatal Respiratory System: Cardiac Tamponade High High
Contractility = SV, ED vol, BP = (CHF)
Lung compliance - 2nd to less alveoli
Chest wall compliance-- floppy ribs Concentric Hypertrophy = Pressure problem = same size SV
FRC 30 ml/kg- Eccentric Hypertrophy = Volume problem = Larger SV
CO:
O2 consumption 7ml/kg/min (adult- 3.5ml/kg/min) Liver 27% Heart 5% (225ml)
Kidney 22% Lungs 100%
Anterior mandible & thyroid: CNS 15% (750ml)
Thyro-mental distance 6.5 cm = ~3 fingerbreadths)
Ventricular Function Curves: Orbital Muscles Degree of protein binding
Contract. C Superior rectus- supraaduction  “look  up”   CN III Water & Gases- Cross
(Dig, Ca++) SVR Inferior rectus- infradduction  “look  down”   CN III H2O soluble drugs & Proteins- NO
(Nipride) ( Preload) Medial rectus- adduction  “look  in”   CN III The Chemoreceptor trigger zone (CRTZ) and the area surrounding
Left A Lateral rectus- abduction  “look  out” CN VI the posterior pituitary have no BBB.
Ventricular Supeiror oblique- look in & down CN IV
Stroke B Inferior oblique- look out and up CN III Four electrolyte disorders that Seizure threshold:↑  Sz  activity
Volume Contract. 1. Hypocalcemia
( Preload) SVR Oculocardiac Reflex: 2. Hypomagnesemia
(CHF, Phenylephrine) 3. Hyponatremia
Afferent pathway = Trigeminal nerve- V
Efferent pathway = Vagus nerve - X 4. Hypernatremia
ECG  manifestation:  ↓  HR,  Junctional  Rhythm,  PVC’s
PCWP Triggered by: traction on extraocular muscles- MEDIAL Conditions  &  Medications  Likely  to  ↓  Sz  Threshold:
Aortic Stenosis Aortic Regurgitation IHSS (HOCM) RECTUS, ocular manipulation, manual pressure on globe Hypoglycemia
HR , SVR , Preload , SVR , HR Keep full, SVR Tx/Blockade: antimuscarinic meds, retrobulbar block, IA Alkalosis
Phenylephrine Rheumatic fever Phenylephrine Demerol is the opioid most likely to cause seizures
Mitral Stenosis Mitral Regurgitation Tetralogy of Fallot ICP: Aminophylline & ketamine together
HR , SVR Preload , SVR , HR Phenylephrine, SVR Normal = 5-15 mm Hg
Focal ischemia – 25-55 mmHg Acute Spinal Shock:
PVR with acidosis & hypercarbia Global Ischemia > 55mmHg Hypotension occurs due to sympathetic blockade and
R L shunt bradycardia due to blockade of cardiac accelerators.
Intracranial Transmural Pressure = MAP-ICP Autonomic Hyperreflexia- T5 or T6
SVR with acidosis & hypercapnia
IC Volume: Cerebral Vasospasm:
Sepsis 80% Brain matter & intracellular H2O 4-12 days post op
↓PCWP                                                ↑  CO                                                                            ↓  SVR 12% Blood S/S: worsening headache, confusion, HTN
8% CSF
Becks Triad (Tamponade) Triple H Therapy:
Muffled heart sounds ICP Waveforms: For treatment of cerebral vasospasm
JVD A waves = plateau waves, found in pts with ICP -Hypervolemia = CVP > 10 mm Hg, PCWP = 12-20
HoTN B waves -Hypertension = SBP 160-200 mm Hg
C waves lesser magnitude -Hemodilution = Hct 33%
Statins -Medication - Nimodipine
Inhibitors of HMG-CoA recluctase Twelve S/S of ICP:
S/E: 1. Liver dysfunction & 2. Severe myopathy 1. Headache Wake-up test monitors the anterior (ventral) spinal cord, which is
2. N & V supplied by the anterior spinal arteries. These are motor tracts.
Protamine dose: 3. Blurred vision
1.0-1.3 mg/100 U Heparin 4. Unilateral pupil dilation Complications of wake-up test:
5. Papilledema 1. Recall
6. Cranial nerve III (oculomotor) paralysis, adduct 2. Extubation
Heparin for bypass: 7. Cranial nerve VI (abducens) paralysis, abduct 3. Dislodgement of spinal instrumentation
300 U/kg 8. HTN 4. VAE from spontaneous ventilation
9. Bradycardia Cushing’s  Triad
10. Irregular respirations In  Parkinson’s  avoid
aVR aVL Initial dose of FFP: 11. Altered LOC Reglan
10-15 ml/kg 12. Seizures Compazine
aVF Droperidal
Antithrombin III deficiency Treatment of ICP: All  meds  that  ↓  Dopamine
give FFP→ 1. Dehydrate the brain with Mannitol (0.25-1g/kg) or Lasix
2. Give steroids- slowest but may restore BBB VAE Doppler @ RA 3rd-6th ICS, R of sternum
3. Hyperventilate to PaCO2 25-30 mm Hg (1/2 life 6 hours) 1. Notify surgeon so they can flood the field or pack
4. Restrict fluids 2. Turn off N2O
Autoregulation: 5. Elevate HOB to 300 3. Administer 100% O2
Cerebral Perfusion Pressure = MAP 50-150 mmHg 6. Administer cerebral vasoconstrictor (pentathol, etomidate) 4. Aspirate central venous catheter to remove air
Coronary Perfusion Pressure = MAP 60-160 mmHg 7. Control BP 5. ↑CVP  (Valsalva  maneuver)
Renal Perfusion Pressure = MAP 80-180 mmHg 8. Cool pt to 340 C for cerebral protection 6. CV drugs to support circulation
7. Bilateral jugular vein compression
Cranial Nerves & Functions: Posturing: 8. PEEP
# Name Function(s) Decordicate: above cerebellum= flexion, upper & exten- lower 9. Position- left lateral decub w/ 15 degree head down
I Olfactory Smell Decerebrate: at brainstem = extension arms & legs, arched body tilt
II Optic Vision CSF:
III Occulomotor Adduction of eye (medial re), pupil size Cranial Fossae: Choroid Plexus
IV Trochlear Eye movements Anterior = Frontal lobe
V Trigeminal Chewing, mastication, Facial sensory Middle = Temporal lobe Lateral Ventricle
VI Abducens Abduction of eye (lateral rectus) Posterior = Brainstem & cerebellum
V Facial Facial muscles, taste (anterior 1/3 tongu Foramen Monroe :
VIII Acoustic Balance (vestibular), hearing (cochlear) Fontanelles Time to Close
IX Glossopharyngeal Taste (posterior 1/3), carotid & sinus af Anterior 18 mos. 3rd Ventricle
Posterior 2 mos.
X Vagus Parasympathetic efferents, HR
Anterolateral 2mos Aqueduct of Sylvius
XI Spinal Accessory Motor control of larynx & pharynx
Posterolateral 2 years
XII Hypoglossal Tongue muscles 4th Ventricle
Specific gravity of CSF = 1.003-1.009
Oh Oh Oh To Touch And Feel A Girls Vagina- So Heavenly Foramen Luschka Foramen Magendie
Hyperbaric- D10
Isobaric- CSF
Cerebral autoregulation MAP 50-150 mmHg Subarachnoid Space
Hypobaric – NS/Sterile H2O
CBF = 750ml/min, 50ml/100g/min, 15% of CO
CBF= CPP/CVR Brain
CSF forms @ 21 ml/hr or 500-700 ml/day in the choroid plexus
CPP= MAP-ICP (RAP)- whichever is higher (80-100mmHg)’
Glucose consumption: 5mg/100g/min Arachnoid Villi
Choroid plexus is located specifically in temporal horn of each
lateral ventricle, the posterior portion of the third ventricle, and
the roof of the fourth ventricle.
CSF is reabsorbed mostly in the arachnoid villi (4/5), but also in
Brain Perfusion Circle of Willis:
spinal villi & lymphatics.
Non Ischemic Ischemic R/L Internal Carotid
Blood Vessel Blood Vessel Basilar & Vertebral Arteries
Total volume: of CSF = 150 ml
Flow diameter Flow Diameter
CSF Pressure: 10 & 20cm H2O
Cerebral 0  Δ  max   Slack Brain
Steal
↑ ↑ ↓ dilated
Aqueduct of Sylvius is the most common site of CSF obstruction
Mannitol/ Diuretics
Inverse 0  Δ  max   Hyperventilation PaCO2 = 25-30mmHg
Steal
↓ ↓ ↑ dilated
Four factors governing passage across BBB:
Hypertonic Saline
Size - smaller crosses easier
Cerebral steal- Hypoventilation (↑CO2) & Vasodialators (Nitro) Head up position
Charge- (ions do not cross- Na, K, Mag)
Inverse- Hyperventilation (↓CO2) Lipid solubility- Cross
Hypotension Interneurons = PAG & nucleus raphe High incidence of ipsilateral hemidiaphragmatic paresis
MAP 60-70mmHg MAP 50mmHg
Maintain  or  ↓  transmural  pressure   Pain categories: Shoulder & humerus = interscalene and Supraclavicular
Results in luxury perfusion –intracerebral steal syndrome Nociceptive: physiologic
carried by A-delta-sharp, prickly & C fibers-dull Cervial Plexus Block:
EEG Somatic-sharp & well localized C1 (motor), C2, C3, and C4 = 4ml
0.1 millivolts (mV) 100 microvolts (V) Visceral-diffuse, dull & vague some plastic surgery procedures, carotid endarterectomy
Brain waves 10-100 microvolts Neuropathic: tracheostomy and thyroidectomy.
Caused by abnormal processing of painful stimuli. Neuropathic Complications: hiccups, Horner’s, hoarse,
Delta: 1-4 Hz- greatest amplitude- sleeping adult, abn in wake pain may occur after injury to neural tissue secondary to systemic
Theta: 4-8 Hz- Amplitude- higher than alpha & beta, but lower disease, infection, trauma, ischemia, deficiencies in metabolism Horners Syndrome= blockage of stellate ganglion @ C7
than delta or nutrition, or exposure to environmental toxins or neurotoxin Least likely w/ axillary block
Alpha: 9-14 Hz- higher in amplitude, alert but relaxed- eyes close medications. Ipsilateral side (same)
Beta: 15-40 Hz- low amplitude, frontal head, business activity [Link] (droopy eye lid)
Variations seen w/ benzo & propofol – mu wave Lateral spinothalamic (neo) tract- most important spinal tract 2. Miosis (pupil constriction)
for pain 3. Facial & Arm flushing (d/t vasodilatation)
Amplitude: Delta >Theta >Alpha >Beta Allodynia: perception of an ordinarily non-painful stimulus 4.  ↑  Skin  Tem  
Frequency: Beta > Alpha > Theta > Delta as pain 5. Anhydrosis (lack of sweating on face)
Hyperpathia is a combined disorder consisting of hyperesthesia, 6. Nasal Congestion
Gamma: high-order activity like problem solving (> 25yo) allodynia, and hyperalgesia
Mu: beta wave variant- seen over motor areas- amplitude ½ of beta Bier Block
Lambda: awake patient that is staring, reading or looking @ objects Neurochemical mechanisms of pain involve different NT: Minimum tourniquet time = 15-20 mins or 20-40
Sub P, Bradykinins & serotonin released → arachononic acid Lidocaine 0.5% or Prilocaine 0. 5% -40 – 50ml
GA:    ↓  high  frequency  in  Beta  waves released = thromboxane, prostaglandins & leukotrines No bupivacaine- ♥  tox  or  chloroprocaine- thrombophlebitis
↑  low  frequency  in  delta  &  theta  waves 300 torr or 2.5 times the SBP
Preganglionic Parasympathetic Nerves originate: Contraindicated: severe crush injuries, uncontrolled hypertension
Surgical stimulation  or  light  anesthesia:  ↑  high frequency, low voltage Cranial nerves III, VII, IX, & X 3,7,9,10 craniosacral Raynaud's disease PVD, Homozygous sickle cell
activity Sacral segments S2-S4
Right Hand: Pronated Supinated
Cerebral compromise & deep anesthesia: low frequency, high voltage Weak Acids: (Thiopental, other barbit, [+ Charge/ Na+, Mg++],
activity Proton Donor 1 = Ulnar 2
Acid + Acid = unionized 2 = Median 1 2
Sevo & Enflurane: can accentuate epileptic activity 3 = Radial
- -
Isoelectric 1.5-2.0 MAC Weak Base: (LA, ketamine, opiods, benzos) [- Charge/ Cl , SO4 ] 3 1 3
Barbiturates, etomidate, and propofol = burst suppression Proton Acceptor Nerves that Flex the Forearm:
Ketamine, opioids and etomidate- do not produce a Δ in latency & Base + Base = unionized Musculocutaneous
amplitude Radial
Ionized = H2O soluble
Spinal Cord: Non-Ionized – lipid soluble (crosses BBB) The Radial Nerve innervates
Sensory – Afferent – Dorsal Horn S.A.D -Posterior Potency = lipid solubility Extension @ elbow, supination of FA, extension of wrist & fingers
Motor – Efferent – Ventral Horn Anterior Duration = protein binding & solubility Damage = inability to ABDUCT thumb & wrist drop
MMEP: Peripheral- popliteal, Central- anterior Speed of Onset = pKa
Preganglionic SNS – Intermediolateral Horn Fetus  pH  <  maternal  pH  =  ↑  ion  trapping   The median nerve innervates:
Pronation of FA, flexion of wrist
Dorsal-Lemniscal (Sensory): Damage ↓amplitude mcg/ml S/S of Lidocaine Toxicity To thumb, index finger, middle finger & lateral ring finger
SSEP Monitoring (posterior spinal arteries) ↑  latency 3 Circumoral Numbness(non CNS- d/t extracellular extravasation) Innervates the medial aspects of FA
Touch, pressure, vibration 4 Lightheadedness Pronator teres
6 Visual Disturbances Flexor carpi radialis
Dorsal (posterior) cord – Cuneatus & Gracilis tracts
8 Muscular Twitching Palmaris longus
Ascend ipsilateral side
10 Unconsciousness Flexor digitorum superficialis
Decussate @ brainstem to contralateral thalamus & sensory
12 Convulsions Damage = inability to ADDUCT thumb & Ape Hand
cortex
15 Coma
Also goes to RAS where it percolates to sensory cortex 20 Respiratory Arrest
Somewhat sensitive The ulnar nerve innervates:
26 Card iovascular Collapse (widen QT precedes) Flexion of wrist, adduction of all fingers
Tibial – electrodes midline scalp, Ulnar- electrodes lateral
The little finger & medial ring finger (C8)
Blood flow highest to lowest- loss of LA d/t vascular reabsorb In the forearm:
Visual evoked potential- CN II- very sensitive to IA In Intravenous Flexor carpi ulnaris
BAEP – CN VIII- barely sensitive (altered most by temp) Time Tracheal Medial ½ of flexor digitorum profundus
Ketamine,  etomidate,  &  opioids,  barbs,  propofol  =  no  Δ  in  latency  or   I Intercostal And in the hand:
amplitude in SSEP Can Caudal Palmaris brevis muscle
Please Paracervical Abductor digiti minimi
Ascending Pain (Anterolateral): Everyone Epidural Flexor digiti minimi
Lateral Spinothalamic Tract (neopalatine) But Brachial Plexus Damage = Claw hand
A- Fibers – Myelinated,  Fast  “first”  Pain  &  temp Susie & Spinal Innervates the adductor pollicis of the thumb
Rexed’s  lamina  I  &  V, dorsal horn Sally Subcutaneous
Neurotransmitter - glutamate
Musculocutaneious
C Fibers – Unmyelinated,  Slow  “dull”  Pain  &  temp Brachial Plexus: Flexion @ elbow
Rexed’s  lamina  II (substantia gelatinosa) & III, dors
Neurotransmitter – substance P Musculocutaneous Nerve
Median Nerve Nerves of Lower Extremity
Interneurons go from II & III to V
Axillary Artery Femoral Sciatic
Epidural steroids
Ulnar Nerve
Both fibers ascend or descend in the tract of Lissauer 1-3 segmnt
Saphenous Common Peroneal Tibial
Both fibers decussate and ascend on the contralateral side. Radial Nerve
Deep peroneal superficial peroneal Sural
Five factors that alter the latency and/or amplitude of SSEP: Right Foot: 4
1. Cerebral perfusion 20 hypotension, PaCO2, ICP “Robert  Taylor  Drinks  Cold  Beer”  =  Root,  Trunk,  Division,  Cord,  Branch
2. Cerebral hypoxia 1 = Tibial Sciatic
R T D C R
3. Hypothermia (MOST) C5 superior lateral musclecutanous 2 = Sural
4. Hyperthermia C6 median 3 = Saphenous Femoral 5 5 2 3 2
5. Hemodilution; Hct < 15% C7 middle posterior axillary 4 = Deep Peroneal Sciatic
C8 radial
5 = Superficial Peroneal
Descending Pain (Dorsolateral): T1 inferior medial ulnar& median
3
Dorsolateral Funiculus – modulates pain
(spinal analgesia) Four Approaches: supraclavicular, infraclavicular, axillary,
top of foot 1
Originate in the periventricular and periaqueductal gray areas and interscalene
Bottom of foot
terminate on enkephalin-releasing interneurons in Rexed’s  lamina  II from hee
(substantia gelatinosa). This inhibits the release of substance P. Axillary: for forearm & wrist, safest, miss the muscultaneous
Functions of nerves of ankle & Foot
(Presynaptic inhibition) 30-40ml,
musculocutaneous = 3-5 mL of LA into coracobrachialis muscle. [Link] = anteromedial foot, medial anterior calf and the
Periventricular Gray Substantia Enkephalin Substance Supraclavicular = greatest risk of pneumo, most compact 40ml dorsum of the foot
Periaqueductal Gray Gelatinosa Interneurons P Less likely to miss the peripheral or proximal branches 2. Deep peroneal nerve= toe extension & sensation to medial ½
All via nucleus magnus raphe in the pons and then descending via Interscalene = shoulder surgery, miss of ulnar nerve & targets 3. Superficial peronal nerve = sensation superficially to dorsum of
the dorsolateral funiculus TRUNKS, no hand 40 ml foot & all 5 toes
4. posterior tibial – sensation to heel, medial sole & lateral sole Isobaric = CSF High Spinal:
5. Sural – sensation to lateral foot Hyperbaric = Dextrose solution C8 = numbness @ little & ring finger
Hypobaric = sterile H2O C7 = numbness @ middle fingers
Flexion of foot= medial plantar & lateral plantar - tibial C6 = numbness @ thumb & index finger
Extension – peroneal nerve Epidural
1-2ml of LA per segment for epidural block Blocks for SAB:
Superficial  :  saphenous,  superficial  peroneal,  sura    “S’s” 13cm needle Sympathetic = 2-6 dermatomes higher than sensory
17 or 18 gauge needles Motor = 2 dermatomes lower than sensory
Femoral Nerve ~ 5cm from skin to epidural space (up to 8cm obese) Progression of blockade: Autonomic>sensory>motor
L2, L3, L4
Anterior thigh & knee Batson's plexus in the epidural space communicates with the 1. Temperature sensation
Anterior muscles of the thigh azygous system- important during times of engorgement which 2. Proprioception (kinesthetic sense)
NAVEL (nerve, artery, vein, empty space, and lymphatics can cause engorgement of the vessels during instances of 3. Motor function
increased abdominal pressure 4. Sharp pain
Obturator nerve 5. Light touch
Provides sensation to the medial aspect of the thigh and motor Caudal
innervation to the adductor muscles located in the medial thigh Sacrococcygeal membrane (injected into epidural space) Type    B  >  Type  Aδ  =  Type  C  >  Aβ  >  Aα
Anatomical landmarks: 2 sacral cornua, the coccyx, and the C type = more resistant to blockade than A & B fibers
On or above knee surgeries: Femoral, Sciatic, Lateral Femoral,
posterior superior iliac spines
cutaneous obturator Sensitivity: large mylenated > smaller mylenated > unmylenated
Complications: pain at site #1, urinary retention, infection
Dosages: (Adult) Childrens
Sciatic S5-L2: 15-25ml 0.5-1.0ml/kg of 0.125-0.25 SAB additives
L4, L5, and S1-S3 S5-T10: 35ml bupivicaine Epinephrine 0.2 to 0.3 mg
sciatic nerve innervates the muscles of the back of the thigh (biceps premature infant: chloroprocaine 1mlg/kg bolus & 0.3ml/kg Clonidine 75 to 100 mcg
femoris, semitendinosis, semimembranosus, and adductor magnus). phenylephrine 2 to 5 mg
1mcg/kg clonidine
As the sciatic nerve continues, it innervates the muscles of the lower prolong the duration w/o resulting significant ♥  changes
leg and foot
Caudal Dose Bupivacaine:
Popiteal Block = sciatic Epidural Steroid Injection
0.5-1.0 mg/kg
Epidural steroid injections provide relief from acute radicular pain
Infant test dose = 0.5 mcg/kg epinephrine
Nerve Injuries when  the  nerve  root(s)  exhibits:  edema,  inflammation  and  ↑  levels
Max dose is 3mg/kg – (bupivacaine)
Primary mechanisms responsible: peripheral nerve injury of phospholipase A2 expression
are transection, compression, stretch, and kinking
Needles
Face mask ventilation – CN 5 & 7 (facial & tongue numbness) Affects unmylenated C fibers
Cutting: Quinke, Pitkin
LMA – SLN or RLN Non-Cutting: Whitacre, Spotte, Greene
Intubation – RLN, SLN, CN 10, CN 12 SAB 24-27G Cervical @ C6-C7 & C7-T1 d/t the largest interlaminar distances
Epidural- 18 to 16G Toughy
Ulnar nerve Lumbar sympathetic block @ L2
Nerve Blocks – 23G
Is the most commonly injured peripheral nerve
in patients undergoing anesthesia Methylprenisone 40-120mg & triamcinolone diacetate 40-80mg
Passage of Needle
More common in those with BMI > 38 & men
Skin
Subcutanous tissue Procedures & Level of Block:
Brachial Plexus Supraspinous ligament will not pass through on paramedian TURP – T 10 C-Section T4
Placement of shoulder braces = acromion ESWL- T4-6 Testicles- T10
Interspinous ligament approach (paraspinous muscle)
Extreme flexion at the thigh can result in injury to the sciatic, Urinary bladder- S2-S4 Tourniquet- T8
Ligamentum flavum
obturator, and femoral nerves. Lower abd – T6 Upper abd- T4
Epidural Space
Dura Kidney – T10-L1 Cysto- T8-T10
Radial Nerve Subarachnoid Uterine – T8-T10 hysteroscopy- T10
Damaged = loss of the ability to supinate the extended forearm, wrist Hip Arthroplasty- T10
drop, abduct thumb, extend the metacarphophalaneal joints Dermatome Landmarks
C1- Completely Motor Conditions that Increased height of spinal block
Common Peroneal nerve. C4- Clavicle T10- umbilicus ↑ abdominal pressure or engorgement of epidural veins:
Most commonly injured nerve of lower extremity pregnancy, ascites, abdominal tumors, kyphoscoliosis,
T4- Nipples L4-L5-Tibia
Most common injured nerve during lateral position ↑ age =    ↓  CSF volume & increase height of spinal blockade
T6- Xiphoid S2-S5-Perineium
3 issues with common peroneal nerve injury
Loss of dorsiflexion of the foot is consistent with injury to the The tip of the 12th rib corresponds with L1 Complications
Foot drop and inability to evert foot The origin of the scapular spine corresponds with T3 Infection: streptococci- spinal , staphylococcus- epidural
The most protuberant cervical vertebra is at the level of C7 Failure of block
Pudendal nerves The tip of the scapula corresponds with T7 Backache #1
Fracture table level of the posterior superior iliac spine S2 Spinal Headache #2
quicker onset = greater dural damage- harder to treat
Sciatic SAB vs. Epidural usually the next day
Protect w/ pillow under knees SAB segmental spread is 10 d/t: mg, baricity, positions of LA ↑  Women > men & Young > old
Injured when patient rotated to semi supine (hips) Tx: bed rest, caffeine, fluids, epidural blood patch (max 20ml)
Epidural spread is d/t volume of LA
Neurologic dysfunction allergic reaction
Saphenous anterior spinal artery syndrome trauma
Neuroaxial Opioids
Inside of knee (litho with strap medially) drug toxicity infection hematoma
1. Hydrophilic: Morphine
Numbness & tingling along medial aspect of the calves total spinal blockade – s/s = dyspnea, resp arrest, HoTN
Slow onset & prolonged DOA
Intrathecal – 0 early respiratory depression
Femoral Arachnoiditis: inflammatory disorder of arachnoid mater
+ late resp depression d/t rostral spread (6-12 hrs)
Decreased sensation LATERAL thigh which surrounds the spinal cord and cauda equina.
Epidural – + early respiratory depression after 2 hours
caused by exposure of the arachnoid membrane to povidone iodine
+ late resp depression d/t rostral spread (6-12 hrs)
Foot drop: Sciatic (lumbosacral, common peroneal), anterior tibial 2. Lipophilic: Fentanyl, Sufentanil, Alfentanil solution, vasoconstrictors, LA, blood, and contrast media.
Hip vag delivery lateral decub feet plantar flex
Fast onset & short DOA
Intrathecal - + early resp depression (2 hrs) Cauda equina syndrome:
Complications of retrobulbar block 0 late respiratory depression s/s:lower back pain, sciatica, motor & sensory loss, & bladder &
Stimulation of the oculocardiac reflex, retrobulbar hemorrhage, bowel dysfunction
Epidural- + early resp depression (2 hrs)
circumorbital hematoma, penetration of the globe, optic nerve trauma, d/t trauma, lumbar disc disease, ankylosing spondylitis, tumors, or
0 late respiratory depression
optic nerve sheath injection, extraocular muscle injury, intra-arterial abscesses in the lumbar area. It has also been associated with
injection prolonged exposure of the cauda equina to high doses or high
Four common side effects of intrathecal opiods:
1. Pruritus (most common) concentrations of LA that cause direct neurotoxicity.
Transtracheal 2. Urinary retention
Blocking of RLN through cricothyroid membrane w/4% lido TNS: transient radicular irritation, pain in the lower back or
3. N & V
Absorbed across mucous membranes (sim to sublingual) buttocks that may radiate to one or both legs after a spinal
4. Respiratory depression
anesthetic
Regional Common side effects of epidural opioids: Mepivicaine & lidocaine implicated & lasts ~ 1 week
High points in spinal canal: High = C3 & L3 Low= T6 & S2 [Link] retention (bup/morphine)
Widest point in space: L2 2. pruritus (morphine) Absolute Contraindications to Regional Anesthesia
Biggest vertebral opening: L5-S1 [Link] @ site 2. Coagulopathy
[Link] of hands & HoTn
Blood supply to SC – single anterior spinal, paired posterior 3. Marked hypovolemia 4. True allergy to LA
Site of action: nerve root (epidural space), nerve rootlets(spinal), 5. Pt. refusal/inability to cooperate 6. Severe Stenosis
C8-T1 = Stellate Ganglion- if  blocked  =  Horner’s  syndrome
spinal cord 7.  ↑  ICP 8. Abruption placentae
Horner’s  syndrome- ipsilateral miosis, ptosis, enopthalamos,
Apnea d/t Hypoperfusion of resp centers in medulla
flushing,  ↑  skin  temp,  anhydrosis,  nasal  congestion
CSF (+) Epidural (-)
Relative Contraindications to Regional Anesthesia Motor Blockade with LA Tests: Sensitivity:
[Link] neurological dz 2. Back disorder (Ankylosis) Minimal: lidocaine 1%, Mepivicaine 1%, Bupivacaine 0.25% SnNOut
3. Heart Disease 4. Surgery above umbilicus Dense: chloro 3% (most), lidocaine %, mepiviaince 2-3%, Sensitivity, Negative, Out
5. Failure to obtain free flow 6. Sepsis etidocaine 1.5%, prilocaine 3%
7. Mobitz type I or II 8. 3rd degree w/o paceer Specificity:
Four anticholinesterases prolong esters: ↓  plasma  pseudocholinesterase SpPIn
Risk & Complications of Regional Anesthesia 1. Echothiophate (irreversible) Specificity, Positive, In
[Link] 2. HoTN [Link] retention 2. Neostigmine
[Link] analgesia 5. Intravascular injection 3. Pyridostigmine Volatile Anesthetics:
6. High spinal [Link] 8. Back pain 4. Edrophonium VP Bld:Gas Oil:Gas FA/FI MAC .70 N2O
9.N/V 10. pain on injection N2O 0.47 1.4 .99 104
Four conditions that plasma cholinesterase: Sally Sevo 170 0.65 53.4 .85 2.1 0.66
Parturient & LA 1. Pregnancy Eats Ethr 175 1.9 98.5 .65 1.68 0.60
SAB  &  Epidural  =  ↑  spread  &  Depth 2. Liver disease (cirrhosis) Ice cre Iso 239 1.4 90.8 .73 1.15 0.50
Related  to  ↓  thoracolumbar  CSF  volume  &  ↑  neural  sensitivity 3. First six months of life Hot Halo 243 2.3 224 .58 0.74 0.29
Hormonal progesterone  in  CSF  may  ↑  segmental  spread 4. Atypical plasma cholinesterase Days Des 669 0.42 18.7 .91 6.3 2.83
Bupivacaine 0.25-0.5% = good sensory but minimal motor
Volatile anesthetics, propranolol, and cimetidine decrease Note! There may be additive effects between the cardiac
Anticoagulants hepatic clearance of amides. (They inhibit Cytochrome P-450) depression associated with Enflurane (or for that matter Halothane)
NSAID, ASA, sub-q or mini dose heparin- No issues and beta-adrenergic antagonists (i.e. Esmolol)
IV heparin – need nml PTT before regional Avoid Beta-blockers with amide LAs:
Hold 1 hr after placement Labetalol & Propranolol Small Vd = fast elimination
Cathetars removed 2-4/hr AFTER last heparin dose Also:
Heparinization 1 hr after catheter removal Digitalis & Ca++ channel blockers potency = lipid solubility = MAC
LMWH- first dose 24 hrs post op (2x daily dosing)
6-8 hs post op (daily dose) Bretyllium is used to treat cardiac toxicity by amides. Oil/gas: measurement of solubility
First dose 2 hours after catheter removal Three reasons to add epinephrine to LA:
Warfin- stop 4 days before surgery & INR < 1.5 1. Prolong the duration of anesthesia Blood Solubility = speed of uptake
Fibrinolytic or thrombolytic – 10 days 2. Systemic toxicity by rate of absorption
Ticlodipine – 14 days 3. Permit use of larger amounts of LA Inhalation agents: solubility = speed of inhalation induction
Clopidorgrel- 7 days ↓  solubility  =  ↑  speed  of  inhalation  induction
GPIIb/IIIA – hold for 4 weeks post operative 1% = 10 mg/ml
Epinephrine = 1:200,000 = 5 mcg/ml Volatile = CBF, CMR
↑  potency  of  LA: Concentration = Amt/Vol C=A/V Ketamine/N2O = CBF, CMR
↑  potency  =  ↑  protein  binding,  ↑  DOA,  ↑  affinity  for  Na  channels,  ↑   Amt = Conct X Vol IV anesth = CBF, CMR
tendency of cardiac toxicity % = gm/100 ml
Vapor pressure of liquid dependent on SOLEY on temperature
↑  #  of  carbons,  +  Halide,  +  ester  linkage,  large  alkyl  on  tertiary  amide Max Dose Epinephrine:
Subcutaneous or Submucosal infiltration: Wrong Agent in Vaporizer :
Bier Block: 2-3 mcg/kg for adults High Low High
Method of anesthetizing a limb by IV injection while blood flow to or 1 mcg/kg on Halothane Low High Low
extremity is occluded by a tourniquet
Minimum: 15-20  mins  (don’t  release  before- local in systemic) 3 mcg/kg for children Percentage of volatiles metabolized:
Max: 40-65 min (usually d/t tourniquet pain) or 1.5 mcg/kg on Halothane Halothane 15-20%
With local anesthetic: Enflurane 2.4%
Local anesthetics: 200-250 mcg Isoflurane 0.2%
Cmin: minimum concentration of LA to produce conduction block or 3-5 mcg/kg Adults Desflurane 0.02%
MOA: non-ionized LA crosses membrane and ionized binds to Sevoflurane 3.0%
receptor to produce effect. (Ca controls Na permeability) *Do not inject epi:in/around end arteries- fingers, toes, ears, penis,
Block rapidly firing nerves > idle nerves nose Cardiovascular Side Effects:
Autonomic > perception of pain/touch/temp > motor > proprioception
Sux = HR, Histamine
+ Na+ Bicarb =↑  speed  of  onset,  intensity  of  block,↓  pain,  ↑  DOA EMLA Cream:
Mivacurium = Histamine
+  Dextran  =  ↑  DOA 2.5% Lidocaine, 2.5% Prilocaine
Atracurium = Histamine
+  hyaluronidase  =  ↑  spread  of  the  LA  into  the  tissue. Biggest barrier = stratum corneum
D-Tubocurarine = Histamine, HR, BP, ganglionic blockade
Psoriasis or  broken  skin  =  ↑  onset &  ↓  duration  (↑  toxicity)
Ester local anesthetics are eliminated by plasma pseudocholinesterase Contact time at least one hour under an occlusive dressing Metocurine = Histamine, HR, BP, ganglionic blockade
except cocaine, which is eliminated by hepatic metabolism. Reaches a depth of analgesia of about 3-5 mm, Pancuronium = HR, BP
Metabolism: chloroprocaine > procaine > Tetracaine DOA = 1-2 hours. Gallamine = HR, BP
↑  likely hood of allergic reactions d/t para-aminobenzoic acid ESTER Max Dose (mgkg) Duration
Benzocaine Na Agent Renal Biliary Metabolism
Tetracaine is hydrolyzed much more slowly by plasma cholinesterase Chloroprocaine 12 (800) 0.5-1 Succinylcholine Neglig Neglig Primary
and is highly protein bound. Therefore it is the most toxic ester local Cocaine 3 (200) Atracurium Neg Neg Primary
anesthetic. Procaine is the least potent ester. Procaine 12 (800) Mivacurium Neg Neg Primary
Tetracaine 3 (200) 1.5-6 Cisatracurium Neg Neg Primary
Cocaine is an ester of benzoic acid and is the only local anesthetic AMIDE Vecuronium Second-20% Primary Second
that produces vasoconstriction. It is also the only naturally-occurring Bupivicaine 3 (175) 1.5-8 Rocuronium Second Primary Second
local. Blocks  epi  uptake:  caution  in  use  of  tricyclics,  MAO’s,   Lidocaine 4.5, 7 w/epi (500,700) 0.75-2
catecholamine metabolism blockers. The max dose is 1.5 Mepivicane 4.5, 7 w/epi (300,500) 1-2
mg/kg Prilocaine 8 (400) 0.5-1
Cocaine & ropivicaine = constriction Ropivicaine 3 (300) 1.5-8 Brain uptake of anesthetics depends on:
Manifestations of hypersensitivity reactions include: 1. Blood solubility
Amide local anesthetics are metabolized by hepatic metabolism. 1. Localized edema 2. Cardiac output
Metabolism: prilocaine >etidocaine > lido > Mepivicaine >Bup 2. Urticaria 3. Alveolar ventilation
Prilocaine is the least toxic amide LA. 3. Bronchospasm 4. Inspired concentration
4. Anaphylaxis
Prilocaine is metabolized to orthotoluidine. Orthotoluidine is an Three ways to speed of equilibrium:
oxidizing agent capable of converting hemoglobin to methemoglobin. Cardiac Toxicity: 1. Inspired anesthetic concentration
Hypoxia, hypercarbia, and acidosis 2. Second gas effect
Bupivacaine is highly lipid soluble and dissociation form sodium Tx: Fluid bolus, rest, pain meds, caffeine, blood patch (10-30cc) 3. Alveolar ventilation
channels are slow. Cardiac toxicity is high.
TNS: Transient Neurological Symptoms Two most important factors for alveolar partial pressure:
Mepivicaine, etidocaine, & bupivacaine = no enhancement w/epi Lidocaine spinals 1. Inspired concentration
Risk Factors: lithotomy, outpatient, knee arthroscopy 2. Blood solubility
Tetracaine, Etidocaine, and Bupivacaine are about equipotent & most Tx: NSAIDs—d/t sensory nature
toxic LAs. Etidocaine causes seizures at a lower plasma Partial pressures
concentration. Etidocaine & Bupivacaine have lowest maximal dose Lipid Rescue: Inspired>Alveolar>Arterial blood>Brain
ranges. 20% Intralipid Note! This order is reversed during emergence when gas is turned
1.2 to 2 ml/kg and then an infusion off.
Monoethylglycinexylidide: an active metabolite of Lidocaine that 0.25/ml/kg/min for 30-60 mins
contributes to toxicity even when lidocaine plasma levels are low The Meyer-Overton Theory explains that the anesthetic potency
Benzocaine: of anesthetic agents directly correlates with their lipid solubilities.
Ester, Weak ACID
May cause methemoglobinia
MAC is  the  “Minimum  Alveolar  Concentration”  of  anesthetic  at  one   Enflurane and Desflurane most depress ventilation. Halothane To figure out ½ Lies and amounts excreted
atmosphere that produces immobility in 50% of patients exposed to a least depresses ventilation. Time ½ Life Amount of Drug
noxious stimulus. MAC is inversely proportional to potency. 0 0 0
Sevoflurane is most degraded by soda lime and Desflurane least. 1 50 (1/2) 50%
MAC ED50 of non-inhalational drugs. 1.3 MAC ED95 2 25 (1/4) 75%
Isoflurane facilitates CSF absorption = favorable effect on CSF 3 12.5 (1/8) 87.5%
There is approximately 1% in MAC for every 1% of N2O delivery. 4 6.25 93.8%
Decrease response to CO2 ventilatory drive
5 3.125 (1/32) 96.9%
Highest Mac 6mos-12mos 6 1.562 (1/64) 98.4%
Fluoride: des =6, iso= 5 sevo=7
7 0.782 (1/128) 99.2%
Seven factors that MAC:
1. Increasing age Steady-state
Point at which the plasma concentration of a drug is in Second messengers:
2. Hypothermia Molecules that relay signals from receptors on the cell surface to
3. CNS depressants equilibrium with all other tissues is the body
target molecules inside the cell
4. Acute ethanol intoxication
Receptors & Drugs cAMP, cGMP, IP3, calcium
5. Alpha-2 agonists (Clonidine)
6. Pregnancy Agonist: affinity and efficacy
Antagonist: affinity for a receptor but lacks efficacy (cannot Proteins
7. Levels of CNS neurotransmitters Albumin = acid
produce  conformation  Δ)
Competitive:  can  be  overcome  by  ↑  concentrations  of  agonist Alpha-1 acid glycoprotein & Beta-globulins = Base
Three factors that MAC:
1. Hyperthermia Non-Competitive:  antagonism  can’t be  overcome  by  ↑  concern
Partial Agonist: bind with the receptor and has some efficacy, but GABA is the major inhibitory transmitter of the CNS. It opens Cl-
2. Hypernatremia ion channels. It hyperpolarizes neurons inhibiting action potential
3. Levels of CNS neurotransmitters it cannot elicit the maximal tissue response
Inverse Agonist: but results in the opposite reaction of an agonist production.

Volatile anesthetics are metabolized in the liver by cytochrome P-450 Barbiturates, benzodiazepines, propofol, and etomidate work
in hepatic microsomes. Zero Order Kinetics
Constant AMOUNT of drug over a constant time primarily on the GABA receptor.
Opens Cl- channel- hyperpolarization
An oxidative trifluoroacetyl metabolite of Halothane is thought to be ASA, phenytoin, ASA
responsible for acute hepatotoxicity in susceptible individuals. Current research also indicates that inhaled anesthetics also work
Reductive liver metabolism occurs with Halothane in the presence of First Order Kinetics on GABA receptors.
hypoxia. Thymol is the preservative in Halothane. Constant FRACTION eliminated per time
1 compartment = albumin
2 compartments = most other drugs Barbiturates
Fluoride is the most clinically important metabolite of Enflurane. Prolong the attachment of GABA to its receptor.
Vd = Q/Cpt=0 Q = quantity of drug injected
Cpt=o = plasma concentration @ time=0 They work in the reticular activating system (RAS).
Inorganic fluoride and chloride are common metabolites of Halothane
Draw line back from elimination phase to t = 0 Sodium Thiopental (acid) is 72-86% bound to albumin. It reduces
and Enflurane. the sensitivity of the central respiratory center to CO2.  It’s  onset  is  
within 10-15  seconds.  It’s  elimination  half-time is 11.6 hours.
N2O is the only inhalational agent without a halogen. Metabolized by redistribution dependent on CO.
α  phase=  distribution
Acceptable levels in the OR: ↓  CMRO2 &  ↓CBF (2nd ↑  cerebral  resistance)
N2O & Volatile together: Inverse Steal
β  =  elimination  phase  
N2O = 25 ppm Reconstitute w/ Sterile Saline (NO LR-precipitate)
Volatile = 0.5 ppm Hyperalgesia
Dose response curve:
Volatile alone: S/S of intra-arterial Thiopental injection:
Potency: determined by the binding affinity of receptors for the
Volatile = 2 ppm 1. Arterial vasospasm with intense pain down the arm
drugs as well as the efficiency of coupling of binding to response
Slope: relationship between dose and effect 2. Blanching of the skin with loss of distal pulses
N2O is metabolized to N2 in the intestine by reductive anaerobic 3. Eventual cyanosis and possibly gangrene
Efficacy: maximum drug effect
metabolism.
Phase I biotransformation: Intra-arterial injection is treated with Phenoxybenzamine
Six contraindications to the use of N2O: (Dibenzyline).
Alter the molecular structure of a drug by modifying an existing
1. Venous air embolism
functional group of a drug.
2. Malignant hyperthermia pH of Barbiturates is > 9.0, pH of 10-11 is often cited.
1. Oxidation
3. Ear surgery (middle ear)
2. Reduction
4. Closed pneumothorax Barbiturates are contraindicated in status asthmaticus and
3. Hydrolysis
5. Potential pneumocephalus porphyria.
-Cytochrome P450 participates in most oxidation and some
6. Bowel obstruction
reduction.
Methohexital is associated with a higher incidence of hiccups than
Four adverse side-effect of N2O: other non-opioid induction drugs.
Phase II biotransformation:
1. Aplastic anemia
Consists of a coupling or conjugation of a variety of endogenous
2. Congenital anomalies Benzos: (base)
compounds to polar chemical groups of the drug.
3. Spontaneous abortion Sedative: effects: the cortex
4. CNS toxicity amnesia: forebrain and hippocampus
Biotransformation often makes drugs more water soluble and
inactive for excretion in the urine or bile. anxiolytic effects:
↓  methionine synthetase- B12 deficiency = no N2O amygdala, hippocampus, & limbic system.
N2O decreases BP and CO when added to high dose opioids. ↓swallowing  reflex  &  upper  airway  reflexes
Six groups of drugs metabolized by Cytochrome P450:
N2O PVR and PA blood pressure due to mild sympathomimetic 1. Barbiturates ↓CMRO2 &  ↓CBF
effects. It will support fire, but is neither flammable nor explosive. 2. Opioids Flumazenil- competitive antagonist of benzos
3. Benzodiazepines
↑  CBF  &  ↑CMRO2 4.  Amide  LA’s
Three renal changes associated with volatile anesthetics: 5. Tricyclic antidepressants Propofol (acid)
1. RBF 6. Antihistamines weak acid
2. GFR 2,6 diisoprorylphenol
3. UO Quantal Dose Response: ↓  SVR  =  ↓BP
Therapeutic Index = LD50/ED50 Liver metabolism 70% & lung metabolism 30%
Halothane least potentiates NDMRs. ED50 is the dose of drug that is effective in 50% of patients. *Caution with soybean & egg allergy
TD50 dose that produce toxic effect in 50% of animals
Isoflurane and Desflurane most SVR, Halothane has little effect on LD50 death to 50% Etomidate: (base)
SVR. Maintains CV stability the best.
Elimination half-time (T ½) = time taken for the plasma It directly depresses the adrenal cortex.
Halothane and Enflurane produce the greatest myocardial depression. concentration to fall by one-half. T ½ is directly related to Vd and It cerebral blood flow, ICP, & CMRO2
inversely related to Clearance (Cl).
Halothane and Sevoflurane most depress the baroreceptor reflex. Venous thrombosis and phlebitis are most likely after etomidate,
(There is no increase in HR despite decreases in BP) Cl = Vd/ T ½ diazepam, and lorazepam.
↑  Vd=  ↑  T1/2                                                        Small  Vd=↓  T1/2
Isoflurane depresses the temperature-regulating center in the Fast CL=short T1/2 Slow CL= Long T1/2 Four potential problems during recovery from etomidate:
hypothalamus. 1. Suppression of adrenocortical response to stress
2. N & V
Isoflurane, Desflurane, and Sevoflurane decrease cerebral metabolic 3. Plasma cortisol concentration
rate. 4. Depressed immune response

N2O alone increases cerebral blood flow & ICP.

Ketamine: (base) Agonist-antagonist opioids 9. Skeletal muscle rigidity
Causes dissociation between the thalamocortical and limbic systems Kappa: provide analgesia 10. Myoglobinuria
by antagonistic actions on the NMDA receptors. Mu: reverse respiratory depression 11. Hypoxemia
Dysphoria is cause by misperception and/or misinterpretation of Naltrexone, naloxone, nalbuphine
auditory and visual stimuli by stimulating the kappa receptor, The earliest sign of MH is ETCO2
antagonizing the muscarinic receptor, and stimulating the sigma Muscle Paralyzation Temperature may increase 1-2 C0 every 5 minutes.
receptor. Eye muscles → extremities→trunk→abd muscles→ diaphragm. Succinylcholine and volatile agents are triggering agents
Recovery is restored in reverse order Masseter muscle rigidity is an early sign of MH.
♥  Effects:  ↑  MAP,  CI,  PAP,  CVP,  HR
Ketamine produces bronchodilitation Facial muscle = diaphragm -1% of children experience masseter muscle rigidity after
↑  airway  secretions- give glyco Abductor pollis = readiness for intubation halothane and succinylcholine administration. CPK > 20,000
Analgesia Recovery from NMB = ulnar nerve confirms the diagnosis after masseter muscle rigidity following
↓  emergence  delirium  in  kids   & higher bioavailability in kids halothane and succinylcholine administration.
MOA NMB: - Halothane-caffeine contracture test is the standard diagnostic test
Opioids: (bases) Site of action is the motor end plate- nicotinic receptors for MH, but it has too many false positives.
Shortest elimination ½ life ALL MR resemble acetylcholine
Remi < Alfent < MSO4</= Sufentanil < Meperidine < fent Eight actions for initial management of MH:
Four NDMRs that release histamine: 1. Discontinue inhaled agents & Sux
Potency 1. d-Tubocurarine 2. Hyperventilate with 100% O2
Sufent > remifent > fent > alfent > MSO4 > Meperidine 2. Metocurarine 3. Administer Dantrolene
3. Atracurium 4. Treat acidosis with NaHCO3 (1-2 mmoles/kg)
Morphine: 4. Mivacurium 5. Body temp to 38 C0
26-36% is protein bound in the adult 6. Replace anesthesia circuit and CO2 absorber
Less is protein bound in the neonate 20 alpha-1 acid glycoprotein. Mivacurium is metabolized by plasma cholinesterase. 25% 7. Monitor ETCO2 & ABGs
Metabolite: morphine-6-glucuronide- prolonged in RF & crosses BBB spontaneous recovery is reached in 13 minutes in adults and 7 8. Treat hyperkalemia and dysrhythmias if necessary
by mass action minutes in children.
Atracurium is eliminated by ester hydrolysis and Hoffman Dantrolene: binds to the ryanodine-1 channel and inhibits the
Meperidine (Demerol) elimination; Cisatracurium is only eliminated by Hoffman calcium channel in the sarcoplasmic reticulum. Decreasing the
myocardial contractility and HR elimination. release of Ca++ from the sarcoplasmic reticulum in skeletal muscle
↓  shivering  - Kappa receptors and causes skeletal muscle to relax. The initial dose is 2.5 mg/kg
↓  sz  threshold  (↑  having  a  sz)    d/t  Normeperidine Hoffman elimination is temperature and pH dependent. The rate followed by 1-2 mg/kg boluses to a maximum dose of 10 mg/kg.
It should be avoided with MAO inhibitors & Imipramine of metabolism is slowed by acidosis or temperature. The therapeutic blood level is 2.5 mcg/ml. Vials of Dantrolene
contain 20 mg and each is mixed with 60 ml of sterile distilled
Adverse S/S of MAO inhibitors & Demerol: Laudanosine is a lipid-soluble metabolite of atracurium that can H2O.
1. Hyperpyrexia ♥  Effects: cause CNS stimulation in high concentrations. It should be repeated every 10-15 hours for three days.
2. HTN ↓  HR,  
3. Hypotension ↓SVR Four MRs that use renal excretion least: Five complications include:
4. Respiratory depression ↓  venous  retur 1. Succinylcholine 1. Reoccurrence
5. Skeletal muscle rigidity ↓  BP 2. Atracurium 2. DIC
6. Seizures 3. Cisatracurium 3. Myoglobinuric renal failure
7. Coma 4. Mivacurium 4. Skeletal muscle weakness
5. Electrolyte abnormalities
Most clinically used opioids are relatively selective for Mu receptors. Three NDMRs not significantly excreted by kidneys:
1. Atracurium Gastric lavage is the best method to Temp with MH.
Lamina II- substania gelatinous of SC 2. Cisatracurium Procainamide, 15 mg/kg is the best antiarrhythmic for MH.
PAG & periventricular area in brain stem = spinal analgesia 3. Mivacurium
The incidence of MH in children is 1:15,000
Spinal analgesia is mediated primarily by Mu-2 receptors, but also Pipecurium is primarily eliminated by renal (70%) and The incidence in adults is 1:50,000
by kappa and delta receptors. Besides the substania gelatinosa secondarily by biliary (20%). The mortality rate is 10%
(Rexed’s  lamina  II),  the  periaqueductal and periventricular gray areas Rocuronium undergoes  no  metabolism,  eliminated  w/  no  Δ  
are important sites of spinal analgesia. Neuroleptic malignant syndrome can mimic MH, but the onset
Supraspinal analgesia is primarily mediated by Mu-1 receptors, but What can augment NMB: and recovery are different. Patients treated with antipsychotic
also by kappa and delta receptors. 1. Hypermagnesium drugs such as Haldol, prolixin, or thorazine are susceptible to
2. Hypocalcemia neuroleptic malignant syndrome. Fever is the cardinal sign
Mu-1 receptors produce: 3. Hypokalemia
(low abuse potential) (Supraspinal analgesia) 4. VA : des > sevoflurane > iso > N2O/fentanyl Anticholinergic:
1. Euphoria 5. Hypothermia 1. Atropine, - most  ↑  HR
2. Miosis 2. Scopolamine- most sedative
3. Bradycardia Eleven possible complications of Succinylcholine 3. Glycopyrrolate - does not cross BBB d/t being a quaternary
4. Hypothermia administration: Combine reversibly w/ muscarinic cholinergic receptors prevent
5. Urinary retention 1. Hyperkalemia acetylcholine from binding to the receptor.
6. Pruritus 2. Bradycardia (Succinylmonocholine-metabolite  @  ♥  SA  Node) Sedative effect: Scopolamine > atropine > 0 glycopyrrolate
3. HR and/or BP Antisialogogues effect: Scopolamine > glycol > atropine
Mu-2 receptors produce: 4. Skeletal muscle myalgia HR: Atropine > glycopyrrolate >scopolamine - < PR interval
(high abuse potential) (Spinal analgesia) 5. Allergic reaction Infants & elderly little effect on HR
1. Respiratory depression 6. Triggering of MH Bronchodilatory effects: Ipratropium
2. Marked constipation 7. Sustained masseter muscle contraction Do not use scopolamine in GLAUCOMA
3. Physical dependence 8. Myoglobinuria
9. IOP (NOT prevented with defasculating dose) Gastric Effects: ↓gastric secretions, ↓ peristalsis and intestinal
Kappa receptors produce: 10. Intragastric Pressure (prevented with defasiculating dose) motility, ↑ gastric emptying time, & ↓  lower esophageal sphincter
(Spinal [Kappa-1] and Supraspinal [Kappa-3] analgesia) 11. ICP (prevented with defasiculating dose) tone.
1. Sedation Five conditions that accentuate succinylcholine-induced Central anticholinergic syndrome:
2. Dysphoria hyperkalemia: Scopolamine & atropine both cross the blood-brain barrier and
1. Unhealed third-degree burns block muscarinic cholinergic receptors in the CNS, producing
Four Ventilatory effects of opioids: 2. Denervation of skeletal muscle restlessness, hallucinations, somnolence, and potentially,
1. Breathing rate 3. Severe skeletal muscle trauma unconsciousness. Predisposed patients: Tricyclic antidepressants
2. Minute ventilation 4.  Upper  motor  neuron  injury  (head  injury,  Parkinson’s,  CVA) (like amitriptyline), antipsychotics, and antihistamines
0
3. Response to CO2 2 brainstem depression 5. Muscular dystrophy (antimuscarinic characteristics)
4. Arterial CO2 tension 6. Renal Failure w/ hyperkalemia Tx: physostigmine
7. Severe Sepsis
Naloxone, Nitroglycerine, and Glucagon can reverse opioid-induced 8. Duchennes Xanthines:
sphincter of Oddi spasm. 9. Guillian Barre Aminophylline & theophylline
cause release of norepinephrine from sympathetic postganglionic
Alfentanil is eliminated faster than all other opioids (except Eleven clinical manifestations of Malignant Hyperthermia: neurons and should be avoided with Halothane.
Remifentanil) because it has a small Vd. The elimination ½ time is 1. Hypercarbia
10-30 minutes. 2. Tachycardia Halothane should be avoided with patients intoxicated with
3. Tachypnea cocaine or using imipramine, because they both block reuptake of
Remifentanil is metabolized by blood and tissue nonspecific esterases. 4. Hyperthermia norepinephrine.
Has glycine buffer- DO NOT use in neuroaxial. 5. Hypertension
6. Cardiac dysrhythmias Calcium channel blockers and volatile agents act synergistically
7. Acidosis (metabolic)
8. Hyperkalemia
Chemotherapy Medications and Site of Toxicity One  PRBC  =  ↑  Hct  3-4% 1g/dl Sickle Cell Disease:
Bleomyocin – Lungs doxorubicin -Heart 1cc/kg  PRBC=  ↑  Hct  1% A hereditary hemolytic anemia resulting from the formation of an
Cisplatin- Kidneys cyclophophains, streptozocin, 1  unit  plts  =  ↑  5,000-10,000 mm3 abnormal hemoglobin (Hb S). Red cell survival is reduced to 10-15
Methotrexate-Liver Massive transfusion = 1 complete blood volume in 24 hours days, compared with up to 120 days in normal individuals.
Immunosuppressive PRBC Sickling occurs only under extreme hypoxemia or in low-flow
3 major risks- 1. Infection [Link] 3. Progressive vascular dz Universal Donor = O Universal recipient = AB states.
Calciumium inhibitors = cyclosporines & tacrolines Platelets The goal of exchange transfusions is to decrease blood viscosity
S/E: HTN, hyperlipidemia, ischemic valve dz, DM, neuropathy, CNS Universal Donor= AB Universal Recipient=O and achieve a Hct of 35-40% with 40-50% normal hemoglobin (Hg
effects A1). Avoid hypo- and hyperthermia, acidosis, and even mild
Coumadin drugs competitively inhibit vitamin K so synthesis of degrees of hypoxemia, hypotension, or hypovolemia. Generous
Calcium Channel Blockers work: Vitamin K-dependent factors (II, VII, IX, and X) is diminished. hydration and a relatively high (>50%) FiO 2 are desirable. Many
Phase 2, plateau phase of ventricular action potential avoid the use of tourniquets.
Phase 4 of the pacemaker action potential Cryoprecipitate is the fraction of plasma that precipitates when
FFP is thawed at 40 C.  (The  drug  of  choice  for  Von  Willebrand’s   Acute chest syndrome – dyspnea, chest pain, hypoxemia
Drugs to avoid with MAO inhibitors: disease)
1. Tricyclic antidepressants (imipramine) Cryoprecipitate contains factors I, VIII, XIII Normal hemoglobin (Hemoglobin A) has:
2. Opioids (especially Demerol) 2 beta globin chains
3. Indirect acting sympathomimetics (ephedrine) Aprotinin inhibits plasmin and therefore inhibits the breakdown & 2 alpha globin chains
4. Fluoxetine of fibrin.
Sickle Cell Anemia is a mutation of the beta globin chains –
Digoxin: (Digitalis) FFP glutamic acid instead of valine
-Enhances myocardial contractility, HR, & slows impulse 10-15mg/kg
propagation through the AV node. Contains all clotting factors but plts Four diseases associated with thrombocytopenia:
-Used to treat CHF & SVT Uses: isolated coagulation factor deficiencies, reversal of 1. Chemotherapy or unrecognized cancer
+ + ++
-Inhibits the Na -K pump causing intracellular Ca accumulation. Coumadin, liver dz- reverse coagulation issues, after massive 2. Liver disease and splenomegaly
-Work by decreasing Phase 4 depolarization of the SA node transfusion and still bleeding 3. DIC
-Hypokalemia, hypercalcemia, and hypomagnesemia increase the 4. Pre-eclampsia
likelihood of digitalis toxicity. Max Allowable EBL:( 20% EBV)
-Hyperventilation should be avoided because it creates a relative Porphyria
hypokalemia. Hypokalemia causes binding of digitalis to myocardial Hct - aHct Hct = 3 x Hbg Metabolic d/o affecting biosynthesis of heme = thick blood
cells, resulting in an excessive drug effect. MABL= EBV X Hct Signs & Symptoms
-Eliminated primarily by the kidneys, 35% daily 1. Acute abdominal pain, N & V
2. Neurotoxicity: confusion, SIADH, difficulty swallowing, HTN
Three side effects of tricyclic antidepressants: PRBC replacement: Hct of PRBC = 75 & tachycardia
(Amitriptyline) 3. Sensory & motor neuropathies
1. Anticholinergic effects (dry mouth, blurred vision, tachycardia) PRBC (ml) = (Blood loss – MABL) x desired Hct
2. Orthostatic hypotension Hct of PRBC AVOID Triggering Agents: KEPT MAN
3. Sedation Barbs Benzos Ketamine Etomidate
Estimated Blood Volume (EBV): Total Body Water (TBW): Nifedipine Ketorolac Enflurane Sulfamides
Tricyclic antidepressants interact with: Premie (< term) 95 ml/kg Adult 60% = 42L Phenytoin Hydralazine mepivicaine lidocaine
1. Anticholinergics (atropine, scopolamine) Term 90 Neonate 80% GA- no regional
2. Sympathomimetics (ephedrine) Infant (< 6 wks) 80 Premie 90%
3. Inhaled anesthetics ( dysrhythmias) Toddler (6 wks-2yrs) 75 Hemophilia : x-lined recessive
4. Antihypertensives (rebound HTN) Child (2 yrs-12yrs) 72 ICF: 60-66% 25-28L A- Factor VIII Deficiency
5. Opioids ( analgesia & respiratory depression) Men 70-75 ECF: 33-40% 14-17L B- Factor IX Deficiency
Women 65 Interstitial fluid 80% Prolonged PTT & normal PT
Anaphylactic Reaction: (Type I hypersensitivity reaction) Plasma water 20% Tx: Factor Concentrates
Antibody Ig E (immunoglobulin E) is produced in response to an Fluid replacement:
antigen (foreign protein). Upon a second exposure to the antigen, Ig E 4 ml/kg first 10 kg (1-10kg) Polycythemia:
on the surface of mast cells and basophils triggers the release of 2 ml/kg second 10 kg (10-20) Abnormal  ↑  Hct   can develop AVWD
mediators including histamine. This causes bronchoconstriction, upper 1 ml/kg remainder (20+) 50-60% Hct = HA Ideal Hct = 33-36
airway edema, vasodilation, increased capillary permeability, and Short cut: Add 40 to your total Kg (if >20) Tx: phlebotomy, avoid dehydration
urticaria. Life-threatening.
Fluids: Heat Loss:
Anaphylactoid Reactions do not involve Ig E. Foreign substances LR: pH 6.5 - contains K 4, Na 130,lactate 28– hypo (osm 273) Radiation 40%>Convection 32%>Evaporation 28%>Conduction
(i.e. drugs, hetastarch) directly stimulate the emptying of mast cells Too much = metabolic alkalosis
and basophils. NS: Na = 154 meq/L = Isotonic (osmol = 308) For each 10 C in body temperature,
Too much= hyperchorlemic acidosis Basal metabolic rate > 7%
Anaphylactic and Anaphylactoid reaction = same S&S D5: Hypotonic (osmolality 252 mOsm)
5% Albumin- colloid osmotic pressure of 20mmHg The center for Heat Loss is located in the anterior (preoptic)
Top 5 Causative of Anaphylactic Reactions Normosol- No Ca++ (osmol 294) hypothalamus and the Heat Gain center is located in the posterior
NMB 60% Hespan: 6% hydroxyethyl starch in NS =/>  20ml/kg/day  =  ↑   hypothalamus.
Latex 17% serum amalayse levels
Abx 15% Hextend- 6% hydroxyethy starch in solution w/ electrolytes, Great decrease of core temp occurs in 1st hour of surgery
Colloids 4% glucose and lactate
Hypnotics 3-4% Operating room temp #1 critical factor min OR temp 21C
Isotonic: ~ 285 mOsm/L- effective osmolality close to body fluid
Latex Allergy CELLS DO NOT SWELL OR SHRINK Hypothermia
[Link] surgical procedures Hypotonic ~ <285 mOsm/L -- ↑  vascular  volume SVR and myocardial depression ( CO)
2. health care personnel Hypertonic ~ > 305 mOsm/L -- ↓  cells  shrink   blood viscosity, left shift of oxyhemoglobin dissociation curve,
3 atopic people w/ hx of multiple allergies +
impaired coagulation, and thrombocytopenia
4. food allergies: bananas, avocados, chestnuts, stone fruit P osm= 2 x plasma [Na ] drug elimination 20 hepatic blood flow and metabolism.
Renal blood flow and clearance slow renal excretion of drugs.
Coagulation: Dextran 40:
Intrinsic Path = XII, XI, IX, VIII (12,11,9,8) Improves blood flow through the microcirculation presumably by Eight Physiologic effects of Hypothermia:
Extrinsic = III, VII (3,7) decreased blood viscosity. Maximal dose = 20 ml/kg/day or
1. O2 consumption ( CO2 production)
Final CP = V, X, I, II, XIII (5,10,1,2,13) about 58 ml/hr for 70 kg patient.
2. SVR
Not in Liver: III, IV, VIII (3, 4, 8) -Side effects of excessive Dextran 40 include: interference with
3. Cardiac dysrhythmias
Vitamin K Dep: II, VII, IX, X (2,7,9,10) blood typing, prolonged bleeding time, renal failure, and
4. Left shift oxyhemoglobin dissociation curve
anaphylactoid reactions.
5. Coagulopathy
Heparin = Intrinsic = aPTT & ACT 6. Blood viscosity
Coumadin = Extrinsic = PT & INR Five adverse effects of Mannitol administration:
1. Pulmonary edema and Cardiac decompensation 7. Impaired renal function
2. Rebound ICP 8. Drug metabolism
Bleeding time 3-10 min. – Platelet function
PT 12-15 sec - extrinsic pathway 3. Hypovolemia
PTT 25-35 sec. – Intrinsic pathway 4. Hyperkalemia
ACT 80-150 sec. 5. Hyponatremia
TT 9-11 sec. – final common pathway
Virchow Triangle
1. endothelial injury
2. stasis or turbulent blood flow
3. hypercoagulability of blood
Natriuretic Peptides Thyroid Storm Six physiologic functions that require Ca ++:
ANP- atrial – from atrial muscle in response to local wall stretch Severe exacerbation of hyperthyroidism 1. Action potentials in smooth and cardiac muscle
BNP- brain- ventricle muscle when distended S/S - 6-8 hrs. post-op 2. Blood coagulation
CNP- endothelial walls 1. Hyperthermia 2. Tachycardia [Link] 3. Bone formation
Urodilitation- lower urinary tract 4. Dehydration 5. Shock 6. Hyperglycemia 4. Muscle contraction
-cGMP- mediates Tx: Na Iodide, cortisol, propranolol, Propylthiouracil 5. Membrane excitability (Ca++ controls threshold)
-Induces  vasodilatation  of  arterial  and  veins  =  ↑  RBF  &  GFR Thryotoxosis d/t sudden excessive release of thyroid gland horm 6. Neurotransmitter release- Ca is REQUIRED
-Suppress actions of NE, angiotensin, endothelin,
-Inhibit – renin, angiotensin II, aldosterone Difficulty breathing after thyroidectomy: A rapid in plasma [Ca++] leads to skeletal muscle spasm
↑  ANP  &  BNP  =  mortality  predicator  in  CHF [Link] edema (laryngospasm) and tetany.
2. Bilateral cord paralysis
Five second messengers: 3. Hematoma formation #1 Nine S/S of Hypocalcemia:
1. cAMP 4. Hypocalcemia 2nd to hypoparathyroidism 1. Numbness earliest d/t neuronal membrane
2. Calcium ions Parathyroid: 2. Circumoral paresthesia irritability
3. Calmodulin Regulates Ca++ & Phosphate 3. Confusion
4. cGMP 4. Seizures
5. Inositol Triphosphate (IP3) Preop parathyroid: correct volume, Avoid LR,  ↑  NDMB 5. Hypotension
6. LV filling pressures (due to contractility)
4 Reasons for difficulty breathing after Thyroidectomy: Parathyroid hormone [Ca++] by: 7. Prolonged QT interval
1. Laryngeal edema 1. Absorption of Ca++ from intestine 8. Skeletal muscle weakness
2. Bilateral cord paralysis 2. Reabsorption of Ca++ from renal tubule 9. Fatigue
3. Hematoma formation 3. Resorption of Ca++ from bone
4. Hypocalcemia 20 hypoparathyroidism Chvostek’s  sign  (contracture of facial muscle with tapping)
Complications of Parathyroidectomy: monitors  hypocalcemia.  d/t  ↑  membrane  excitability,  closer  to  
Six hormones of the Anterior Pituitary: (Adenohypophysis) 1. Hypocalcemia RMP
(Blood flow through Hypothalamic-Hypophyseal Portal System) 2. Parasthesias More  excitable  d/t  Δ
1. Adrenocorticotropic hormone (ACTH) 3. Muscle spasm of threshold closer to RMP ECG changes with Hypocalcemia:
2. Thyroid stimulating hormone (TSH) 4. Tetany 1. Prolonged QT interval
3. Growth hormone (GH) 5. Laryngospasm 2. ST segment duration
4. Prolactin 6. Bronchospasm 3. Flat or inverted T-waves
5. Leutinizing hormone (LH) 7. Apnea
6. Follicle stimulating hormone (FSH) 8. Hematoma Functions of Magnesium:
9. Airway compromise (It both resembles and antagonizes Ca++)
2 hormones of the Posterior Pituitary: (Neurohyphosis) 10. Pneumothorax 1. Functions as a cofactor in many enzyme pathways
[Link]-Diuretic hormone (ADH) 2. Regulates the Na+/K+ pump
2. Oxytocin Major postop concern after Parathyroidectomy: 3. Regulates adenylate cyclase
(Airway obstruction) 4. Regulates slow Ca++ channels
Thyroid: Laryngospasm 20 hypocalcemia 5. It antagonizes Ca++ (an endogenous Ca++ channel blocker) =
Regulated by TSH release from anterior pituitary Bilateral recurrent laryngeal nerve damage vasodilatation
93% Thyroxine (T4) Hematoma 6. Controls the threshold potential (membrane stabilizer)
7% Tri-iodothyronine (T3) 7. Regulation of the release of acetylcholine from nerve terminals
Ca > 5.5 mEq/L
About 80% of Tri-iodothyronine is produced outside the thyroid gland Ionized Ca++ >2.5 mEq/L Hypermagnesemia:
by de-iodinazation of thyroxine. Signs & Symptoms
Osteitis Fibrosa Cystica is a bone disease caused by 1. Coma
Tri-iodothyronine (T3) is four times more potent than thyroxine (T4). hyperparathyroidism. Leaking of Ca out of bones= broken and 2. Hypoventilation
brittle bones 3. Hypotension
T4 is converted to T3 in the tissues
Calcitonin promotes the deposition of calcium in the bones and ↑  Mg  =  ↓  excitability  
Thyroglobulin = protein decreases [Ca++] in the ECF. (opposite of PTH)
Caused from: excess dietary intake of Mg, excess ingestion of oral
Serum thyroxine levels < 1 mcg/dl → severe hypothyroidism and Clinically significant hypocalcemia: antacids, hypothyroidism, hyperparathyroidism, Addison's disease,
warrant delay of an elective case or treatment with thyroid hormone ECG changes (prolonged Q-T interval) & lithium therapy
prior to emergency surgery. Myocardial contractility
Tx: forced diuresis with saline and loop diuretics
Normal serum thyroxine levels is 5-12 mcg/dL S/S of hypocalcemia following parathyroidectomy:
1. Perioral parasthesias Hyperphosphatemia
S/S  of  Grave’s  Disease: (Hyperthyroidism) 2. Restlessness Impairs coagulation by causing platelet dysfunction
1. Intolerance to heat 3. Neuromuscular irritability Impairs ventricular contractility & leukocyte function
2. Sweating Chvostek’s  sign
3. Mild to extreme weight loss Trousseau’s  sign Causes of hypophosphatemia:
4. Varying degrees of diarrhea Inspiratory stridor 1. Ingestion of large # antacids containing aluminum & Mg
5. Muscular weakness 2. Severe burns
6. Nervousness Five complications of RRP: 3. DKA
7. Extreme fatigue 1. Hemorrhage 4. ETOH WD
8. Inability to sleep 2. Compromised ventilatory function 5. Prolonged respiratory alkalosis
9. Tremor of the hand 3. Air embolism Tx: aluminum based antacids, Carafate, Ca citrate, dialysis
10. Exothlamous 4. Damage to obturator nerve 20 retractors
5. DVT Eight signs of Hyponatremia: [Na+] < 135 mEq/L
Beta antagonist is the drug of choice for treating hyperthyroid-related (Normal [Na+] = 138-146 mEq/L)
ventricular dysrhythmias. Four effects of acidosis on CNS function: 1. Arrhythmias 2. Hypotension
1. Depressed neuronal activity (coma) 3. Pulmonary edema 4. Mental changes
Four causes of Hypothyroidism: 2. Cerebral vasodilation ( CBF, ICP) 5. Muscle cramps 6. Weakness
1. Subtotal lobectomy of thyroid 3. Cerebral perfusion pressure (cerebral ischemia) 7. Myoclonia 8. Edema
2. Goiter +
4. Seizure threshold S/S develop with [Na ] < 120 mEq/L
3. Autoimmune disease (myxedema) Treatment is with diuretics and hypertonic saline
4. Radiation therapy of thyroid Anion Gap: = [Na+] – [Cl-] – [HCO3-] Hypernatremia = dehydration
Can cause cretism in infant = large tongue Normal range = 9-15 mEq/liter
Used in the differential diagnosis of metabolic acidosis. Three factors that promote Hypokalemia:
Hypothyroidism: (Normal extracellular [K+] = 3.8-5.0 mEq/L)
S/S Four causes of metabolic acidosis: 1. Alkalosis
1. Slow mental function 1. Ketoacidosis 2. Insulin
2. Slow movements (weight gain) 2. Lactic acidosis 3. Beta-2 adrenergic stimulation stimulates Na-K
3. Dry skin 3. Renal failure pump3Na:2K
4. Cold intolerance 4. Toxic dose of salicylates
5. Depressed ventilatory responses
Metabolic Alkalosis
6. Abnormal cardiac conductivity ( cardiac function) 1. Vomiting
7. Renal disease 2. NG suctioning
3. Hypokalemia 20 diuretics
↓  Anesthesia  requirements  – however,  no  Δ  in  MAC
The kidneys excrete H+ as titratable acids H2PO4 & NH4+
Plasma K+ approximately 0.6 mEq/L for each 0.1 in pH
Seven ways to treat Hyperkalemia: GFR: nml 95-150ml/min, mild dsyfx 50-80, mod dsyfx <25, Epinephrine (80%), norepinephrine (20%), and dopamine are
1. Give calcium gluconate failure <10 ml/min catecholamines released from the adrenal medulla.
2. Give glucose/insulin This is controlled by sympathetic preganglionic neurons that
3. Give sodium bicarbonate Nephron Sections: release acetylcholine to nicotinic receptors.
4. Give diuretics (to increase excretion) 1. Glomerulus: freely filters Na, Cl, K & H2O
5. Give kayexalate (potassium exchange resins) 2. Proximal tubule: 67% of glomerular filtrate- reabsorbed 3 Stimuli for the release of Renin:
6. Use hemodialysis H2O > Cl > Na = K, ONLY place permeable to glucose 1. Renal perfusion pressure Normal GFR = 125 ml/min
7. Hyperventilate the patient Filtration, reabsorption and secretion 2. Hyponatremia
Plasma [K+] is 0.5 mEq/L for each 10 mmHg in PaCO2 3. Descending LOH: Urea & H2O (no Na, Cl or K) 3. Sympathetic NS stimulation of beta-receptors in JG apparatus
Osmotic gradient via countercurrent multiplier
+
Cardioplegia – 15-40 mEq/L of K 4. Ascending LOH: Filters Na, Cl, K – No H2O in thick branch Clinical features of Diabetes Insipidus:
Loop Diuretics – Na+, K+, 2CL- inhibit reabsorption Polyuria, > 2-15 L/day- HALLMARK
Calcium should be given to the hyperkalemic pt. when ventricular SE:  ↓  K,  fluid  volume  deficit,  orthostatic  HoTN,  reversible   Hypernatremia (plasma hyperosmolality)
dysrhythmias  appear.    (↑  threshold  away  from  RMP) deafness (CNVIII) Dilute urine (osmolality < 200 mOsm/kg)
Lasix  ↑  prostaglandins=  venodilitation  =  ↓BP Neurogenic vs. Nephrogenic – give ADH to Dx
Medications  that  cause  an  ↑  K 5. Distal Tubule: Filters Na & Cl (No K or H2O)
Triamterene, spironolactone, NSAIDs, ACE inhibitors, BB Early:  Thiazides:  ↓  K S/S of Diabetes Insipidus:
Late  &  CC:  Potassium  Sparing  Diuretic:  ↑  K 1. Polydipsia ( thirst)
ECG  Δ  with  Hyperkalemia   Triamterene, amiloride Spiratalctone 2. Polyuria – (2-15L/Day) HALLMARK
Prolongation of P-R interval ADH & Aldosterone 3. Hypernatremia
Widening of QRS [Link]:Na & Cl-out, K-In, Low perm H2O, (no urea) 4. Hypovolemia
Peaked or tented T waves Site of Action ADH & Aldosterone (principle cells) 5. Hypotension
6.  ↓  Urine  osmol  (<200  mosm/kg)
Cortex: Glomeruli, Proximal Tubules, Distal Tubules 7.  ↓  specific  gravity  (1.005  or  less)
ECG  Δ with Hypokalemia
Medulla: loops of Henle, Collecting Ducts
Prolongation of P-R & Q-T interval
Flattening of T waves Diagnosis of SIADH: ↑  ADH (intracranial tumors)
*Inner stripe of the outer medulla= most vulnerable to ischemia Decreased plasma osmolality (< 270 mOsm/kg)
Appearance of prominent U wave +
urine [Na ] (> 100-150 mOsm/kg)
Carbonic Anhydrase Inhibitor: Hyponatremia d/t retention of H2O
nd
Addison’s  disease: glucocorticoid & mineralocorticoid deficient Acetazolamide(Diamox)-↓  IOP  2 to  ↓  aqueous  humor  formation Tx: remove underlying cause, Limit H2O , 3% Saline, demecolcine
Hypoadrenocorticism- autoimmune destruct of the adrenal cortex Inhibit carbonic anhydrase in proximal  tubule  =  ↓  Na  
S/S reabsorption = diuresis – Hyperchorlemic Metabolic Acidosis Liver: 25% CO
1. Hypotension Blood Flow:
2. Hyponatremia ↓  Aldosterone Mannitol: 70% Portal vein - splenic & mesenteric 50:50
3. Hyperkalemia ↑  Osmotic pressure  in  renal  tubule=  ↓  reabsorption of H2O 30% Hepatic artery Oxygen supply
0 +
4. Hypoglycemia (2 cortisol levels) S/E:  ↓  K  
5.  Hemoconcentration  (d/t  to  ↑  H2O excretion 2nd to hyponatremia) “Arterial Buffer Response”
6. Skin pigmentation Renal Failure: An increase in hepatic arterial flow in response to a decrease in
Give glucocorticoid intraop S/S  &  lab  findings  normal  until  40%  ↓  in  Fx portal blood flow (1) to maintain hepatic O 2 supply, and (2) to
FENA Urine Sodium (mEq/L) maintain total hepatic blood flow, which is essential for clearance
Cushing’s  disease: Prerenal Failure <0.01 (1%) < 20 of many compounds.
Hyperadrenocorticism- ↑  cortisol  &  ↑  ATCH  in  anterior  pituitary Renal Failure > 0.03 (3%) >40
nd
1. HTN (2 to Na retention) Hepatic Blood Flow
2. Hypokalemia Anuric: UO <100ml/day or < 0.5ml/kg/hr Arteries:  α-1,  β-2, D1 &cholinergic =blood flow receptors: Ohms
0
3. Hyperglycemia (2 cortisol levels) Oliguric: UO 100-400 ml/day 30% of Blood flow, 50% of oxygen supply
4. Moon face & buffalo hump NonOliguric: UO >400ml/day Veins:  α-1 & D1- blood flow depend on GI & Spleen
5. Skeletal muscle weakness 70% of blood flow, 50% of oxygen supply
6. Skin pigmentation Electrolytes:  ↑  K,  Mg,  Phos,  ↓Ca , Na , metabolic acidosis
Seven functions of the Liver:
Conn’s  Disease: Infection is # 1 issue and cause of death 1. Storage and filtration of blood (500ml)
Primary hyperadolteronism 2. Metabolic functions such as carbo, fat, and protein metabolism
↑  Na+ Fenoldapam  DA1  agonist:  ↑  RBF    (6x  more  potent  than  dop) 3. Secretion of bile
↓  K+ 4. Storage of vitamins
Avoid Meperidine & Morphine (metabolite-6) 5. Blood coagulation
Pheochromocytoma: 6. Storage of iron
Tumor  of  the  adrenal  medulla  chromaffin  tissues  which  results  in  an  ↑   ADH: (vasopressin) : NA+ Concentration 7. Detoxification & excretion of drugs
catecholamine release Synthesized Periventricular and Supraoptic nuclei of the
S/S: hypothalamus, stored in and released from the posterior pituitary P450’s
1. Paroxysmal HTN (neurohyposis). Inducers: chronic ETOH, barbs, ketamine,  benzo’s,  phenytoin,  
2. Diaphoresis 1. 10 on collecting ducts in the nephron = passive water cigarette smoke, St. Johns wort
3. Tachycardia reabsorption
4. Headache 2. Vascular smooth muscle and cardiac myocytes. Inhibition: cimetidine, chloramphemocel, fluoxetine, grape fruit
Tx: [Link] vasoconstriction and has an inotropic effect Bile vomitus is usually alkaline. This is because large amounts of
α  block- phenoxybenzamine 20-30mg/day  &  ↑  to  60-250mg/day, alkaline phosphatase are normally excreted in the bile. A three-fold
β  block- tx for tachy Released in response to ECF osmolarity, plasma volume, & or greater increase in alkaline phosphatase is indicative of biliary
Avoid: Trimethaphan, droperidal, histamine drugs, stress, HoTN, Pain, CPAP, PEEP, VA, Trauma tract obstruction.
Works in the distal tubule & collecting duct to H2O Puke your acids = alkalosis
Multiple Endocrine Neoplasia: (MEN) reabsorption, In the absence of ADH the collecting duct and Poop your bases = acidosis
A group of syndromes characterized by tumor formation in several distal tubule are impermeable to H2O ie: excretion happens.
endocrine organs. Alcoholic Hepatic Issues/Liver Disease
MEN I = tumors in pancreas, pituitary gland, & parathyroid gland ADH = Osmolality = [Na+] (concentration) Thrombocytopenia, leukopenia, anemia, megoblastic anemia d/t
MEN II = medullary thyroid carcinoma, pheochromocytoma, and folate deficiency
hyperparathyroidism (type IIa) or multiple mucosal neuromas (type Extra Cellular Fluid Volume: Na = ECFV +
↑  MAC
IIb or type III) DT’s  24-96 (1-4 days)
0
1. 1 on collecting ducts in the nephron = passive water Maintain BP- ETOH depends on ARTIERAL FLOW
Kidney: 25-30% CO reabsorption Isoflurane- agent of choice
Functions: 2. Vascular smooth muscle and cardiac myocytes. ↑  Vd=  ↑  loading  dose,  smaller  main  =  prolonged  Vec,  Roc,  Pan  
[Link] composition: Osmolality: 285-305 mOsm/kg [Link] vasoconstriction and has an inotropic effect Labs:  ↑  total  bilirubin,  ↑AST/ALT  (ALT  more  sensitive),                          ↓  
Urine osmolality 50-1200 mOsm/kg H2O albumin & PT
2. Maintenance of EFV- NA & H2O excretion Aldosterone: VOLUME Hemodynamics:  ↓SVR,  ↑CO,  ↑circ  blood  volume,  ↓portal  blood  
3. Endocrine: It controls intravascular volume and works in the collecting duct flow,  ↓  plasma  osmotic  pressure
Erythropoietin- CRF = anemia and the late distal convoluted tubule.
RAA System- BP reg, Na/K excretion Increases Na+ reabsorption (conserved), and K+ secretion Increased surgical risk in Liver Failure patient
Vitamin D: CRF = hypocalcemia (excretion). 1. High bilirubin >3.0 mg/dl
4. Regulation of arterial BP Release is triggered by Angiotensin II and [K ]; also ACTH 2. Low albumin < 3.0 mg/dl
+
+ +
and low serum Na . It also regulates the total amount of Na . 3. Severe ascites
RBF = (MAP- Venous Pressure) x Vascular resistance Aldosterone (a mineralocorticoid) is secreted by the zona 4. Coma 5. Poor nutrition
Autoregulation – MAP 75-160 mmHg glomerulosa of the adrenal cortex. Mendelsons Syndrome: (aspiration pneumonitis)
Filtration ceases MAP <60mmHg Cortisol (a glucocorticoid) is secreted by the zona fasciculata, the Gastric pH < 2.5
middle zone of the adrenal cortex. Gastric volume <25 ml
Labs: Creatine Clearance is single best indicator of renal status
Creatine: 0.7-1.5 mg/dl BUN: 10-20mg/dl
Seven conditions that delay gastric emptying: Carcinoid Syndrome Muscular Dystrophy
1. Obesity S/S caused by vasoactive substances released from Painless degenerative & atrophy of skeletal muscles
2. Pregnancy enterochromaffin tumors or carcinoid tumors Duchene’s (most common & severe)- x-linked, recessive
3. Opiods Most carcinoid tumors are in GI tract- especially appendix EKG- prolonged PR, QRS, ST abnormalities, BBB, Q waves, R
4. Diabetes mellitus Cause overproduction: serotonin-hallmark, bradykinin, waves (tall), CHF
5. Trauma histamine, kallikrein, prostaglandins Resp: ↓TLC & RV, recurrent pulm infections
6. Pain NO  succs  (↑MH)
7. Anxiety **Avoid activating tumor: HoTN, catecholamine release,
histamine releasing medications Multiple Sclerosis- MS
Drugs  that  ↓  LES  Tone: (↑  risk  of  aspiration) *HoTN- volume expanders Random & multiple sites of demyelination of corticospinal tracts
1. Anticholinergics, *right sided  ♥  failure in brain & SC (NO PERIPHERY)
2. Dopamine No spinals (may exacerbate)
3. Thiopental Five clinical manifestations of nonintestional tumors: Avoid – rises in temps
4. Opioids, 1. Cutaneous flushing Hyperkalemia in response to Succs
5. Propofol, 2. Bronchospasm
6. Tricyclic antidepressants 3. Diarrhea Parkinson Disease
7. Sodium nitroprusside. 4. Large BP swings Loss of dopanergic fibers basal ganglia (dop is a inhibitory NT)
5. Supraventricular dysrhythmias s/s: skeletal muscle rigidity, resting tremor, diaphragmatic spasm
Patients who benefit from antiemetics: **you  don’t  see  this  with  intestinal tumors d/t first pass Tx: Levodopa
1. Eye surgery patients metabolism in the liver Levadopa S/E: dyskinesias, hallucinations,  paranoia,  and  mania.  ↑  
2. Gynecological patients in cardiac contractility & HR. Orthostatic HoTN & N/V
3. Obese patients Octreotide (somatostatin) used to blunt vasoactive and Avoid: droperidal, reglan, Compazine
4. History of vomiting bronchoconstritive effects of carcinoid products
5. ECSW Lithotripsy Rheumatoid Arthritis
Pancreas: Endocrine Chronic inflammation disease w/cervical vertebral involvement
Antiemetics: Beta cells: insulin Restrictive lung disease, pulmonary fibrosis, FOB, pulm fx test
Competitive Dopamine Antagonists; Alpha cells: glucagon Hoarseness or stridor – Cricoarytenoid involvement
Droperidal, Compazine, Metoclopramide Delta cells: somatostatin ♥  Δ’s- pericardial effusion, aortic regurg, cardiac valve fibrosis,
Do  not  give  to  Parkinson’s  Patients   anemia,
Evaluation of pancreatitis:
Droperidol: 1. Malnutrition Cyanide Toxicity: Cyanide binds to cytochrome oxidase resulting
1. An antiemetic (20 dopamine blockade) 2. Abnormal liver FX in inhibition of oxidative phosphorylation causing inhibition of cell
2. Produces extrapyramidal signs (20 dopamine blockade) 3. ETOH WD (alcoholism frequent cause of pancreatitis) respiration. (Nitroprusside)
3. May BP (20 weak alpha blockade)
Symptoms of pancreatitis: Myasthenia Gravis- MG
Treatment for droperidol-induced extrapyramidal symptoms is an 1. Dehydration Chronic autoimmune @ NMJ, weakness
anticholinergic (Benadryl or benztropine, Cogentin). 2. Hypocalcemia Ptosis & diplopia – most common initial s/s
3. Hyperglycemia Cardiomyopathy & hypothyroidism
Do not give to: Pheo or Parkinsons 4. ARDS Tx: steroids, anticholinesterase meds, plasma phoresis
Alcoholism is a frequent cause of pancreatitis. Surgery: Thymectomy
Metoclopramide: (NO  Δ  in  pH) Avoid muscle relaxants
1. Relaxes pyloric sphincter 5 “F’s”  of  Cholelathiasis
2. Promotes gastric motility =  ↑  gastric  emptying 1. Fat 2. Female 3. Fertile 4. Forty 5. Fair Lambert-Eaton Syndrome Myasthenic Syndrome:
3. Lower esophageal sphincter tone =  ↓  reflux A disorder of neuromuscular transmission associated with
4. Relaxes the small intestine Insulin is not needed by brain or RBC to utilize glucose carcinomas. An autoimmune disease in which immunoglobulin G
5. Has antiemetic actions (IgG) antibodies against voltage-gated sodium channels cross-react
Insulinoma: with calcium channels at the neuromuscular junction. The result is
It also inhibits plasma cholinesterase Insulin secreting tumor causing massive insulin release. a decreased release of acetylcholine in response to nerve
Tx: tumor resection- Childs Procedure stimulation. Increased sensitivity to NDMRs and succinylcholine is
Used to treat: Hypoglycemia- during resection seen.
Diabetic gastroparesis Hyperglycemia- after resection
Reflux esophagitis Check Blood sugar every 15 mins ↓  Weakness with  ↑  activity
Pts. at risk for aspiration pneumonitis (Mendelsons syndrome)
Parturients Diabetic Neuropathy Ankylosing Spondylitis:
40-50% of IDDM A familial d/o associated w/ histocompatibilityantigen HLA-B27.
Drugs that gastric pH and gastric volume: (H2 blockers) Anesthetic considerations: orthostatic Hotn, Silent MI, Low back pain associated w/ early morning stiffness young men
1. Cimetidine (Tagamet) **inhibits P-450 the most Gastroparesis progressively restricted movement of the spine.
2. Ranitidine (Zantac) ** most potent HR response blunted w/ use of antimuscurinics - Atropine Some patients develop arthritis of the hips and shoulders.
3. Famotidine (Pepcid) ♥  issues Stress steroid dose if needed
Hypoglycemia
Ranitidine gastric volume & pH the most S/S: Diaphoresis, HTN, Hunger, feeling of impending doom Lupus
characteristic manifestations: antinuclear antibodies, nephritis,
Inhibits the cytochrome P-450 system. A1C = 6% serositis, thrombocytopenia, or a characteristic rash.
Cimetidine>Ranitidine>Famotidine=0 S/S: symmetric arthralgias hands, wrists, knees, and ankles,
DM with autonomic neuropathy 65% insulin dependent doesn’t  include  spine.    33%  - Cognitive dsyfx
Drugs that interact with Cimetidine: 3 Anesthetic concerns
1. Propranolol 2. Labetalol Orthostatic Hotn, silent MI, Gastroparesis Complications of TURB:
3. Diazepam 4. Halothane [Link] Loss 2. Hypothermia
5. Lidocaine 6. Phenytoin 6 Cardiac Concerns 3. bactermia 4. Bladder perforation
7. Coumadin 8. Aminophylline Orthostatic Hotn, Resting tachycardia, absence of beat to beat
9. Meperidine 10. Quinidine variability in HR, dysrhythmias, silent MI, painless myocardial Peritoneal Invasion – Sign and symptoms
11. Tricyclic antidepressants 12. Ca++ channel blockers ischemia Awake Patient General Anesthesia
Sudden, severe, abd pain Unexplained HTN (HoTN
Proton Pump Inhibitors: HR response blunted in these medications: rare)
Omeprazole- inhibits the hydrogen pump - =  ↓  secretion  of  HCl  into   Antimuscarinics & Beta-Blockers Should pain Tachycardia
the lumen of stomach NV
*most  powerful  agent  for  ↓  acid secretion MOA of DM neuropathy: High concentrations of glucose are Abdominal rigidity
converted to sorbitol within nerve via the polyol pathway. The high
levels  of  sorbitol  (and  fructose)  that  develop  ↓  ATP→ ↓  NO  levels.   TURP
Antacids:
Because nitric oxide acts as a vasodilator, the loss of nitric oxide leads Preference  for  SAB:  ↓  blood  loss,  ↓  thrombus  risk,  atonic  bladder,  
Raise gastric pH by neutralizing HCl also  ↑  gastric  volume
to unopposed vasoconstriction and ischemia of the nerve prevents postop bladder spasms, awake pt. can assist detecting
Immediate Effect
Thymus issues
Non-Particulate – better for aspiration risk; however, loose Where T-Lymphocytes mature
effectiveness after 30-60 mins Thymus is most commonly removed d/t Thyoma & MG Complications:
Pneumo most likely on RIGHT side [Link] Loss 2. Venous absorption of irr fluid
Chemoreceptor Zone: Thymic vein drains into innominate vein
4th ventricle (area posterema) 3.  venous  sinuses  of  prostate                          4.↑  intravascular  volume
5. Dilutional hyponatremia 6. Bactermia
Scoliosis 7. hypothermia 8. Coagulopathy
Neurotransmitters & Receptors in N/V: Lateral curvature of the spine
Dopamine & DA-2 Restrictive lung dz- ↓  VC,  TLC,  IV,  FRC,  IC,  ERV
Serotonin & 5-HT
FEV1/FVC = normal Deliberate Hotn MAP 60-65
Acetylcholine & muscarinic Mitral valve prolapse Anticipate blood loss
Substance P & NK-1
Nonelectrolyte Solutions for TURP Cor Pulmonale Neuro: Spinal Cord Dural Sac
hypotonic/nonelectrolyte ECG sings of cor pulmonale = peaked P waves in leads II, III, NN L3 S3
Glycine 1.5%–↑glycemia  =  temp blindness, ammonia tox, N/V, and aVF which are consistent with right atrial hypertrophy & >1 y.o L1 S1
HA,  ECG  Δ,   right axis deviation and right bundle branch block which are Motor cortex- unmylenated and poorly developed until 2 years
Sorbitol- 2.7% consistent with right ventricular hypertrophy. Sensory cortex- mylenated @ birth, nerves poor develop until 3
Mannitol- 0.54% mos.
Surgical Stimulation CBF 40ml/100g/min (adults 100/100/g/min)
Fluids can cause bladder distension & toxicity Intubation > upper ab surgery > breast surgery = lower ab = skin Neuro surgery: PaCO2 → 20-25 mmHg
incision > skin closure
Bladder Perforation during TURP –Signs & Symptoms: Thermo:
[Link] pain & spasm ASA classes Non-shivering thermogenesis (inhibited by: IA, BB, fent, prop)
Suprapubic fullness 1-Healthy Best way to maintain infants body heat = heat up OR to 26C (78.8)
HTN & tachy—followed by sudden & severe HoTN 2- mild systemic disease- HTN, DM, Anemia, age, obesity, O2 consumption 2x an adults
chronic bronchitis Other:
TURP Syndrome 3- severe systemic disease- Cardiac dz with limiting activity, Large volume of distribution 2nd to higher total body water content
Triad of S/S: ↑  PP,  bradycardia,  mental  status  Δ Uncontrolled HTN, DM w/vascular issues, MI or Angina Higher ratio of body surface area to body weight
Other  symptoms:  HTN,  CV  collapse,  ↑  CVP,  Dyspnea,  N,  anxiety 4- incapacitating systemic dz – CHF, persistent angina, advanced
kidney or liver dz Cardiac Variables:
Tx: Give O2, notifiy surgeon, invasive monitors, blood to lab, 12-lead 5- moribund pt. – Not expected to live 24 hours after surgery- MAP = Gestational Age
ECG, PE, AAA, cerebral trauma Hypotension: SBP NB < 60 1 year < 70 > 1yr 70 + (age x 2)
6- brain dead- organ procurement
Central Pontine Myelinolysis - complication from TURP syndrome- E- not elective- i.e appy ETT:
d/t the rapid tx of hyponatremia Diameter: 4 + Age /4 (cuffed) Premie: 2.5,Infant: 3.0,3-12 mos: 3.5
Mallampati 3 + Age/3 (uncuffed) 3.0 3.5 4.0
Management: stop resection, Labs, fluid restriction, Lasic, NS3% Class 1 – Pillars, soft palate, fauces, uvula, Length: 10 + age/2 10 11 12
Amount of NS 3% = Dose (mEq) = kg x (140-(Na)mEq/L) Class II- Uvula, soft palate, fauces
Stop NS 3% when NA > 120 Class III- Soft palate, uvula Wt. in Kg LMA Cuff vol ETT FOB
+
Na Levels: Class IV- Hard Palate NN- 5 1 4 cc 3.5 2.7
120 mEq/L = restlessness & confusion, (psbl. wide QRS), N/V 5-10 1.5 7 4.0
115 mEq/L = nausea, somnolence, ECG ’s (wide QRS, ST ECT 10- 20 2 10 4.5 3.5
elevation) 1st – parasympathetic- HoTN,  ↓HR    2nd- sympathetic- HTN,  ↑HR 20-30 2.5 14 5.0 4.0
110 mEq/L = seizures & coma with VT, VF ↑CBF  =  ↑ICP          Medication  of  choice:  Brevital  (0.5mg/kg) 30 3 20 6.0 5.0
Desired Duration = 30-60 seconds, sz sec needed= 400-700
**Irrigating fluid = 20ml/min of surgery time Absolute contraindications: French Suction Catheter:
**Blood loss is ~ 3-5ml/min of resection time 1. Pheo Neonate: 8 Fr, 2mos-2yrs: 10 Fr, 2-12 yrs: 14 Fr
2. Recent MI (4-6 wks)
Gas Embolism – laparoscopic surgery 3. CVA <3mos Precordial Stethoscope: 3rd-4th intercostal left of sternal border
S/S:  HoTN,  Tachy,  bilateral  wheezing  &  ↓  ETCO2 4. recent intracranial surgery- <3mos
Halt insufflation, eliminate N2O, release pneumoperitoneum, place in 5. Intracranial mass lesion Medications:
LEFT lateral decub, aspirate gas via central venous cath 6. Unstable C-spine Propofol Midazolam
Relative contraindications: angina, CHF, Pacer/ICD, pulm dz, < 2 y.o = IV induction 3-4 mg/kg. IV dose = 0.05mg/kg
Signs of Fat Embolism during Surgery: major bone fx, glaucoma, retinal detachment, thrombophlebitis, >2 y.o. = 2.5-3 mg/kg PO dose= 0.5 to 0.75 mg/kg
1. ETCO2 pregnancy 200-300mg/kg/min GA
2. PaO2
3. PA pressure Anesthetic goals: partial NMB to prevent long bone fx & Flumazenil Thiopental
4.    ↑  PaCO2 unconsciousness IV 0.05 mg/kg → 1 mg total 4-6mg/kg
5.  ↑ETN2 Succinylcholine = ↑  intubate  dose   NDMR
6.  Late  signs:  ↓  BP,  ↑  HR,  cardiac  dysthymias, cyanosis, mill wheel Fetal Circulation: IV 2-3mg/kg Same dose as adults
murmur IM 4mg/kg
RA RV PA Lung Parallel Circulation Myalgia,  myoglobinemia,  ↓  HR
Fat Emboli Syndrome – 12-72 hrs Foramen Patent ↑  PVR  &  ↓  
SVR ↓  R  to  L  shunt
4 major signs: axillary, subconjuctival petechial, hypoxemia, Prematurity:
Ovale Ductus
↓CNS,  pulm  edema Less than 60 weeks post conceptual = > risk of post anesthesia
LA LV Aorta Body
5  minor  signs:  HR  >100,  pyrexia,  retinal  fat  emboli,  jaundice,  renal  Δ comp
Lab  features:  fat  microglobumia  (required),  ↑serum  lipase,  anemia,   Elective surgery: at least 60 weeks post conception
2 arteries-deoxygenation blood & 1 vein- oxygenated
thrombocytopenia,  ↑  ESR ROP- retinopathy of prematurity: vasoconstriction of retinal
Hemoglobin levels are lowest at 3 months of age 10-11mg/dl vessels- leading to permanent scarring, blindness and retinal detach
Triad: hypoxemia, mental confusion, petechial
Basal metabolic rate is highest at 2 years of age < 44 weeks (post conception)
Prophylaxis: corticosteroids – limiting endothelial damage by FFA
Oxyhemoglobin curve: Newborn= Left shift, Right @ 3-4 mos.
Tx: supportive Causes: Hyperoxia, hypercarbia, Hotn, Sepsis
Inspiratory pressure more negative than 25-40 to open alveoli
Maintain PaO2 60-80mmHg O2 sats 89-94%,
RDS-hyaline membrane disease, 50-75% mortality rate d/t result
S/S of Intraop PE:
of inadequate surfactant in the alveoli
Sudden acute dyspnea! Breathing Patterns:
1. Hypotension Periodic breathing
Premie: less than 37 weeks
2. Tachycardia Recurrent pauses in ventilation no longer 5-10 seconds. During
Neonate: less than 30 days of age
3. Hypoxemia, SpO2 REM sleep not associated with any physiologic disorder.
Infant: 1-12 mos. of age
4. Bronchospasm Central Apnea
Children: 1-12 years of age
5. Hypocapnia, ETCO2- 1st sign d/t dead space ventilation Unexplained cessation of breathing > 15 sec or shorter resp pauses
Post conceptual Age = gestational age + post maternal age
6. PVR > 300 w/ HR < 100, cyanosis, pallor or loss of muscle tone. Premies.
7. + D-dimer Most important risk factor of postoperative apnea
Apgar scores: 1 min = survival & 5 min = neurologic outcome
Rhabomylosis Congenital Heart Issues:
Differences in body systems in Pediatrics: Foramen Ovale Ductus arteriosus
Skeletal muscle necrosis d/t tissue injury Cardiac:
Myoglobin: oxygen transport protein MOA 1.↓  PVR  &  ↑  pulm   ↑  PaO2 &  ↓  
CO of NN & infants is dependent on HR 2nd fixed SV &
Common causes: major crush injury, thermal or electrical injury, flow prostaglandins
noncompliant & poorly developed L vent, depends on Ca++
arterial occlusion, acute muscle injury, prolonged immobility, 2.  ↑  SVR  =  ↑  L  vent   ↑  SVR  &  ↓  PVR
Innervation: Sympathetic = SPARSE, parasympathetic-complete
compartment syndrome, MH, extreme lithotomy, hyperlordotic pressure  =  ↑LAP
position Functional soon after birth 2-4 days
Respiratory: Anatomical 2-3 mos. 1-4 mos.
↑  RR,  ↓  Lung  compliance  +  ↑  chest  wall  compliance  =  ↓  FRC  (↑  
Surgical Lumbar Sympthathectomy Shunt Right to Left Left to Right
IA induction), Deficient in Type I fibers, high closing volumes
To improve blood flow to ischemic areas: causalgia, Raynaud’s, MOA RAP > LAP RAP > LAP
Anterior and cephalad larynx (C3-C4), Adult C4-C5
frostbite, gangrene, ischemic ulceration of lower extremities Problem Cyanosis ↑  work  of  left  side  of  
Obligate nasal breathers
L2-L3 ♥  → Left ventricular
Cricoid cartilage narrowest point in children less than 5 yrs.
Cyanide Toxicity hyertrophy
MAC highest 6 mos. of age
Metabolic Acidosis IV induct Faster Slower
Cardiac arrhythmias Inhal induc Slower Faster
Kidney:
↑venous  O2 content Incomplete glomerular  development,  ↓  size  of  glomerulus  ↓  
Tachyphylaxis RAP > LAP (causes of return or continuation of fetal circulation)
perfusion  pressure,  ↓  ability  to  concentrate  urine,  obligate  Na  
Tx: Na Thiosulfate 150ml/kg over 15 mins 1. Hypoxia 2. Hypercarbia
losers
Myocyte = muscle cell 3. Acidosis 4. Hypothermic
Complex Regional Syndrome 5.  Coughing,  bucking  &  Valsalva                ↑  PVR  or  ↓  SVR  
Hepatic:
Type 1 & Type II (causalgial- previous nerve injury documented) Immature hepatic biotransformation,  ↓  protein  binding,  fetal  liver  
Tx: physical therapy, gabapentin, tricyclics ETCO2 underestimates AaCO2
=  hematopoiesis,  ↑  risk  of  hypoglycemia,  ↓  LBF
Preductal Monitoring : Right Hand or Finger Necrotizing enterocolitis: normal value represents a high-risk state that should be
Postductal: Left foot or toe Most common surgical emergency in the neonate corrected prior to initiating a neuraxial anesthetic.
ABG’s  best  obtained  from  Right  Artery   Premature infants @ > risk for developing Platelet < 100,000 too low to perform a neuraxial anesthetic
Decreased mesenteric blood flow = ischemia → intestinal
Neonatal Coarctation of the Aorta mucosal injury Anesthetic  considerations  w/  Δ:
Narrowing of the descending aorta. If severe – perfusion is dependent *Foreign body aspiration is most common pediatric surgical Smaller ETT ↑  risk  of  failed  intubation
on open PDA shunt. PGE1 use to maintain patency emergency Avoid intranasal manipulations ↑  Minute  ventilation  
BP monitoring in Right Radial artery required
Encephalocele, Meningocele, Myelomeningocele: Do  not  hyperventilated  =  ↓  maternal  alkalosis  =  ↓  uterine  blood  
Congenital Diaphragmatic Hernia (CDH) Neural Tube Defect- abn fusion of embryologic neural groove flow
Foramen of Bochdaleck or anterior foreman of Morgagni Encephalocele: herniation of brain & meninges through defect in GA = RSI 8 wk. gestation to 6 week of postpartum
Larger on left & 90% of diaphragmatic hernias on left. skull producing a fluid filled sac 2nd to  venodilitation  =  ↑  risk  of  accidental  epidural  vein  puncture
Maintain preductal saturation > 85 w/ PIP < 25 cm H2O Meningocele: hernia protrusion of a saclike cyst of meninges VA off after delivery to promote uterine tone
Keep them breathing filled w/ CSF & no neurological deficits- Appendectomy is the MOST common surgical procedure
Decompress stomach and avoid barotrauma Myelomeningeocele: (spina bifida) hernial protrusion of saclike Most common cause of maternal death during GA = Hemorrhage
R to L shunt – monitor pre and post ductal perfusion cyst containing meninges, CSF & portion of spinal cord ↓  MAC  &  ↑  sensitivity  to  LA  
Cyanosis, Dyspnea & Dextrocardia LATEX precautions & Positioning is key
Pharmacology:
Tetralogy of Fallot Inguinal hernia: H2 antagonist & or metoclopramide & nonparticulate
1. Large single ventricular septal defect Nerves blocked: ilioinguinal and iliohypogastric Uterine relaxation: nitroglycerin 50-500 mcg IV or MAC 1.5-2.0
2. Aorta that overrides the right & left ventricles DO NOT give esmolol to PIH/HELLP parturient
3. Obstruction to right ventricular outflow Glucose: Maternal alkalosis & fetal  acidosis  =  ↑  fetal  ion  trapping  
4. Right ventricular hypertrophy Hyperglycemia is neuroprotective for global ischemia in NN
Hypoglycemia can be more detrimental β2: relaxes smooth muscles & stops contractions via activation of
RIGHT to left shunt adenylyl  cyclase  =  ↑  cAMP  =  myometrial  relaxation  
Goals: maintain  volume  status  and  SVR  (need  to  ↑  =  NEO) Tonsillectomy: S/E: cerebral vasospasm, chest pain, nausea, pulm edema, tremor
↑  Blood  loss- 4ml/kg Ritodrine—issues: hypokalemia, hyperglycemia, tachycardia
TEF: Tracheoesophageal Fistula 3 complications: bleeding, laryngospasm & emesis Terbutaline – more likely to have arrhythmias
Most common form ends in blind pouch & lower esophagus that
connects to trachea – C (then B & E) NPO Guidelines Tocolytics
Associated with VACERTL syndrome Substances Minimum Fasting Hours Methergine: exerts  uterine  effect  @  α  adrenergic  receptors,  
Principle cause of death = pulmonary complications Solid Food 8 0.2mg/IV or intramyometrially
↑  secretions                                                                      No  PPV  prior  to  intubation Commercial Formula/Milk 6 Hemabate:  ↑  prostaglandins  F2    (safer  than  meth)  0.25  IM/metral)
Breast Milk 4
Pyloric Stenosis: Clear Liquids 2 Uterine Blood Flow 800ml/min (10% maternal CO)
Infants: projectile vomiting & visible peristalsis 1. ↓ Perfusion pressure: supine, hemorrhage/hypovolemia,
Adults: Peptic ulcer scarring Mendelsons Syndrome: HoTN, contractions, sz, Valsalva
Hyperchorlemic metabolic alkalosis- ↓Cl,  K,  Na,  Ca Volume > 0.4ml/kg or pH <2.5 2. ↑ Uterine Vascular resistance: catecholamines, vasopress
↑  Aldosterone  secretion
Regional Anesthesia: ↑  UBF  from  regional:  pain  relief,  ↓  SNS  activity,  ↓  
Cleft palates & esophageal reflux
Tx: surgical pyloromyotomy Spinal & caudal most common hyperventilation
Anesthetic Considerations: correct electrolytes, rehydration, OG CSF volume x2 of adults = dilution of LA  =  ↑  dosing  &  ↓  DOA ↓  UBF  from  regional:  HoTN,  absorbed LA, unintentional IV inject
Spinal: L3-L4 – distance ~ 1 cm *Maternal BP is only factor influence blood flow through
Post op complication- respiratory depression
High spinal – decreasing oxygen saturation #1 sign placenta
Caudal: tip of coccyx to fix the midline & sacral cornua on *uterine blood flow is NOT autoregulated
Down’s  syndrome  (trisomy  21)  Concerns:
1. Difficult intubation: use small than usual ETT either side of sacral hiatus *α  adrenergic  receptors  predominate  uterine  vasculature
Large tongue Volume determines height of block
Short neck 1.2-1.5ml/kg analgesia T4-T6- concentration no > 2.5 mg/kg Greatest risk to fetus from Maternal issues:
Small mouth Epidural Blood Patch: 0.3ml/kg Severe hypoxia, HoTN, acidosis
2. Neck flexion- Cervical spine dislocation- antlanto-occipt Mepivicaine is not metabolize in the NN
Instability & Weak ligaments Three layers in placental membrane:
Laryngospasm: 1. Fetal trophoblasts
3. Congenital heart disease (40% incidence)
1. CPAP- 10-15cm H2O 2. Cytotrophoblasts
2. atropine 0.02mg/kg 3. Syncytiotrophoblasts
Omphalocele vs Gastroschisis:
Omphalocele Gastroschisis 3. Succs 1mg/kg IV or 4mg/kg IM
Incidence 1 in 5,000 1 in 15,000 Placental Exchange:
Maternal Physiological & Physical Changes: 1. Diffusion: small ions, respiratory gases, most anesthesia drugs
Location Base of umbilicus Lateral to umbilicus
Cardiac: under 1000 Daltons cross,
Anomalies Yes – Cardiac No
Presence of Sac Yes No ↑  CO, SV, HR, LVEDV, EF, Femoral venous pressure 2. Bulk flow, how water crosses the membrane
Infection, hypothermia & ↓  PVR,  MAP,  SBP,  DBP,  SVR, PADP, PCWP 3. Active transport and transfer of AA, vitamins, calcium, & iron,
Hydration more of a concern CO  ↑  the  most  immediately  post-partum 4. Pinocytosis, larger molecules such as immunoglobulins cross
Both: decompress stomach with tube, no nitrous, hydrate 8- ↑  Renin  &  angiotensin  II  x12   5. Breaks in the placental membrane
16ml/kg/hr, if PIP > 25-30 H2O – no primary closure
Respiratory: Placental Transfer of Drugs:
↑  IRV, TV, IC, DS, MV (↑  50%), AV, O2 consumption (↑  33%),   1. Concentration gradient
Epiglottitis vs. Croup
PaO2  >  100,  ↓  MAC,  RR  (10%) 2. Molecular weight of drugs – MW < 500 = easier transfer
Epiglottis Croup
↓  ERV,  RV,  FRC (20%), chest wall excursion, chest wall, FEV1 3. Lipid solubility- lipids soluble drugs = easier crossing
Importance Emergency Non-emergency
compliance Respiratory Alkalosis CO2 = 30, restrictive lung 4. Ionization – ions inhibited
Onset Rapid, 24 hours Gradual 24-72 hours
↑  Alveolar  vent  &  ↓  FRC  =  ↑  inhalation  agent  uptake  &  ↓  MAC VA transfers easily muscle relaxations DO NOT
Radiograph Thumb sign (swollen) Steeple sign (narrow)
Age 1-7 y.o Most <2 yo
Cause Haemophilius B- Flu Cold (viral) GI: Maternal supine hypotensive syndrome:
Fever Yes- HI Low grade Metabolic Acidosis – HCO3 = 20 Compression  inferior  vena  cava  =  ↓  venous  return  =  ↓  SV  &  Hotn
Respiratory Inspiratory stridor Croupy  cough  “bark”   ↑  Gastric  emptying  time   &      ↓  LES          → 2nd to  ↑  progesterone S/S:  diaphoresis,  N/V,  Δ  in  cerebration,  dizzy,  vertigo,  ↑  HR,  apprehension
↑  Gastrin  production   Tx: LUD (i.e Right hip up) 150
with inspiratory stridor
Tube Size ½ size small w/ leak ½ size smaller Definitions:
Tx Ampicillin &/or Epi neb, O2, cool Hepatic:
Albumin ↓  4.5 g/dL to 3.3 g/dL =  ↓  COP  by  5mmHg First stage: Regular uterine contractions until cervix fully dilated.
vaccine before 2 yrs humid, steroids Latent- Cervical effacement 2-3 cm
Anesthesia ~Do not attempt to If  ↑  PaCO2 –intubate ↓  Plasma  cholinesterase  
Active – frequent contractions 3-5 mins & dilatation
visualize glottis Epi Neb- 2.25% in 3ml
Renal: is 4 cm in a primiparous patient & 3 cm in a
~sedate while sitting NS @ 0.05ml/kg up to
↑  RBF & GFR (50%) → ↓  BUN  &  serum  creatinine multiparous patient.
0.5ml/kg q 1-4 hr
↑  Kidney  size  &  weight  &  ureters  and  renal  pelvis  dilates  
Glucosuria & proteinuria Second stage: From the end of the first stage until the delivery of
Cystic Fibrosis: the baby is completed.
Hereditary disease of exocrine glands of resp and GI
Cl- transport  ↓  w/  ↓  Na  &  H2O transport Hemostasis:
Relative hemodilutional maternal anemia, Third stage: From the delivery of the baby until the placenta and
↑  Thickness  of  secretions=  avoid  antisialogogues
Hgb > 14 w/PIH or HTN = low volume the membranes are expelled.
↑  RV  &  airway  resistance,  ↓  VC  &  exp  flow  rate
No ketamine 2nd to increase secretions ↑  Blood volume, plasma volume, RBC, Hbg 11.5 Hct 35.5
↑  Factors 1, 7, 8, 9, 10,12 , Fibrin degradation products, plasminogen Polyhydramnios: excessive amniotic fluid around unborn infant
Shortened  or  ↓:  PT,  PTT,  AT, Factors 11 & 12
No  Δ  2  &  5,  platelets,  bleeding  time
PT, PTT, and bleeding times that are greater than twice the
Pain Pathways for Stages of Labor Regional Opioids Pregnancy Induced Hypertension: (↑  thromboxane  A2)
First stage: uterine contractions & cervical dilatation. Pain travels via Intrathecal Epidural HTN  =  ↓  CI  &  ↓  blood  volume            
visceral afferent fibers accompanying sympathetic nerves. Enter cord Morphine 0.5-1mg 7.5-10mg Gestational hypertension: HTN w/o edema or proteinuria
at T11 & T12 → T10, T11, T12, & L1 spinal segments. Meperidine 10-20mg 100mg Preeclampsia: HTN w/proteinuria and edema during pregnancy.
C-Fibers Fentanyl 10-25mcg 50-100mcg Eclampsia: preeclamptic patient w/ sz
Sufentanil 3-10mcg 10-30mcg HELLP: form of preeclampsia characterized by hemolysis,
Second stage: Caused by distention of lower vagina, vulva, and elevated liver enzymes, and a low platelet count.
perineum. Pain travels via the Pudendal nerves and enters the cord at Pudendal block *uterine blood flow decreases
S2, S3, & S4 sacral segments. (T10-S4 dermatomes) Placed through sacrospinous ligament- via Transvaginal * avoid ketamine
approach ↓  PCHE  – 33% eclampsia & 60% in HELLP = careful dose of
Third Stage: delivery of baby until placenta & membranes out 2nd stage of labor Succs
Risks: hitting the scalp
Paternal Pain Agents in Parturient S/S Severe PIH:
Meperidine: Most commonly used opioid – longed DOA- give in Paracervical Block BP 160/110 Proteinuria 5 g/day
early labor (4 hours before delivery) 10-25 mg IV, 25-50 mg IM Anesthetizing nerve fibers innervate uterus, cervix, upper vagina Oliguria, < 500 ml/day Pulmonary edema
Fentanyl: maternal respiratory depression- 50-100mcg/hr. Submucosally  in  the  vagina  @  3  &  9’oclock Hepatic tenderness or HELLP syndrome
Butorphanol: partial agonist- no resp depression 1-2 mg IV/ IM 1st stage of labor CNS manifestations: HA, visual disturbances, or seizures
Nalbuphine: partial agonist- no resp depression 10-20 mg IV/ IM Risks: Fetal Brady (33%)
Promethazine: can be used with Demerol – 50-100mg IM Complications of PIH:
Ketamine: 10-15mg IV- no LOC, up to 1 mg/kg (> = fetal depress) Signs of Fetal distress: Cerebral hemorrhage- #1 death Pulmonary edema- #2 death
Naloxone directly to the neonate at a dose of 0.1 mg/kg IM Repetitive late decelerations Renal failure Cerebral edema
NO NSAID: they inhibit uterine contractions & promote closure of Loss of beat to beat variability associate w/ late or deep decels DIC Airway obstruction
the fetal DA. Sustained FHR < 80 BPM Fetal Scalp pH < 7.2
Meconium-stained amniotic fluid IUGR Complications that necessitate delivery:
Fetal Heart Tracings: Oligohydramnois SBP >/= 160 or DBP >/= 110 – 24-48 hrs
Early Decelerations (Type 1) Progressive renal dysfunction
Etiology: head compression or stretching Maternal Death progressive thrombocytopenia
of neck during uterine contractions. Most common (most to least) Liver dysfunction
Start & end w/ contraction & UNIFORM Hemorrhage, embolism, preeclampsia, infection & premonitor signs of eclampsia
Mild decrease in FHR < 20 BPM cardiomyopathy Evidence of fetal jeopardy

Late Decelerations (Type II) Uterine Atony Actions of Magnesium:

Etiology: uteroplacental insufficiency & Inadequate uterine contractions following delivery Beneficial:  Anticonvulsant,  vasodilatation,  ↑  UBF,    ↑  RBF,  ↑  
fetal  compromise  w/  ↓  HR Risk factors: multiple gestations, fetal marosomia, prostacyclin,  ↓  ACE,  ↓  renin  activity,  tocolytic  &  bronchodilitation
Onset: begin or near end of contraction prolonged/rapid labor, tocyotlitcs, VA, retained placenta, Detrimental:  ↓  FH  variability,  myoneural  blocking  effects,  
Uniform in appearance + or - variability chorioamniotis generalized  muscle  weakness,  ↑  sensitivity  to  MR
SEVERE: if FHR > 45 BPM S/S: vaginal bleeding and boggy uterus MOA:  ↓  presynaptic  release  of  AcH  &  ↓  post  synaptic  sensitivity  
TX: bimanual compression, uterine massage, IV pic, preeclamptic patients & works @ NMDA → ↓  SVR  &  ↑  CI.
Variable Decelerations: hysterectomy
Etiology: cord compression IV load = 4g over 15-20 mins → 1-4g/hr IV gtt
Nonuniform with variable waveform Chorioaminoitis
Typically associated with fetal asphyxia One of the most common infections during pregnancy MgSO4 Levels:(mEq/L) to convert to mg/dl
when: > 60 bpm FRH, duration > 60 Based on S/S Temp > 38 = CARDINAL symptom 1.5-2 Normal Divide by 0.8
seconds or pattern persists > 30 mins 4-8 therapeutic
Severe:  FRH  ↓  60  by  BPM,  FHR  <  60  BPM  or  decels  60  secs  +   Uterine Cord Prolapse: 5-10 long PR, wide QRS
Fetal bradycardia & late decelerations = fetal hypoxia (asphyxia) May lead to fetal hypoxia 10 lose DT reflex
Dx: sudden fetal bradycardia or profound decels w/ physical 15 respiratory paralysis, SA & AV block
Obstetrics & Regional Anesthesia exam 20 CV arrest
SAB  ↓  dose  by  25%  d/t  ↓  epidural  space  2nd venous congestion &/or Tx: immediate steep trendelenburg or knee to chest position
progesterone-induced sensitivity Magnesium: drug of choice sz prophylaxis in PIH
Antepartum Hemorrhage: Tx for Mg overdose : Calcium Gluconate
Most common S/E = Hotn Placenta Previa:- No Pain
The partial or total covering of the cervical os by the placenta Hydralazine: useful in pregnancy—mainstay
The diagnosis of abruption placentae with or without fetal First bleeding episode – usually preterm w/ no contractions BP
distress is a contraindication to regional anesthesia Painless vaginal bleeding during 2nd or 3rd trimester Uteroplacental BF
Marginal, total, partial- cesarean section
Paravertebral lumbar sympathetic block: used during 1st stage of Avoid vaginal exams Heart Disease in the Parturient:
labor when traditional neuraxial analgesia is contraindicated ↑  incidence  of  asymmetric  IUGH     Group One: mitral valve dz, aortic insufficiency, L to R shunt
Regional Anesthesia: especially continuous epidural
Chloroprocaine: quickly metabolized no opportunity to accumulate Placental Abruption: Pain NEO
in any significant amount. Separation of the placenta from deciduas basalias before delivery Group Two: AS, R to L shunt, primary pulm HTN
Acute bleeding from exposed vessels= lot of BLOOD Regional anesthesia CONTRAINDICATED
Ropivacaine: 1/3 less motor block than bupivacaine & causes less Coagulopathies:  ↓  plts,  factor  5  &  8,  ↑  fibrin  split  products  
CNS & cardiac toxicity, 0.08-0.15% can be administered via an Major complications: hemorrhagic shock, ARF, coagulopathy VAE in the parturient:
epidural catheter at a rate of 8-12 mL/hour to provide continuous One of the most common causes of fetal demise. Place in slight reverse trendelenburg w/ L lateral tilt of 150
analgesia during labor Definitive Tx: delivery of fetus
Four findings that suggest DIC:
T4 level sufficient for caesarean section Abnormal Placental Implantation 1. Thrombocytopenia 2. Prolonged PT
Placenta accrete: placenta adheres to the surface of the 3. Prolonged PTT 4. Serum fibrinogen, Fibrin split
Injuries: myometrium w/o invasion or passage through uterine muscle products
Dorsiflex to foot= common peroneal nerve Most common indication for hysterectomy
Loss of sensation to lateral thigh = lateral femoral cutaneous Placenta increta refers to placental implantation within the DIC is associate with 3 OB problems:
Most common nerve injury during ab hyster= femoral nerve myometrium (confined to myometrium)\= 1. retention of dead fetus
Nerve injury most common w/ vaginal delivery= lumbosacral Placenta percreta refers to the condition where the placenta 2. Placental abruption
completely penetrates the myometrium or other pelvic structures 3. AFE
SAB Doses: Lido 5% 50mg/ml (50-75mg) T7-C8
Bupivacaine 0.75%- 7.5 mg/ml (12-15mg) T5-C8 Amniotic Fluid Embolism: AFE 3rd cause of Lab Tests for DIC:
Tetracaine 1% 7-10mg in D10- hyperbaric T7-T5 death Normal OB DIC
Amniotic fluids into maternal circulation Plasma fibrinogen 400-650 mg/dL <150 mg/dL
Epidural Doses: 1.5-2% Lidocaine S/S: tachypnea, cyanosis, shock, generalized  bleeding,  ↓  CO,   Platelet count 150,000-300,000/mm3 <50,000/mm3
0.5% bupivacaine acute PE, uterine atony, ARDS, arrhythmias, bleeding, SZ Thrombin time 15-20 sec >100 sec
3% chloroprocaine Tx: aggressive cardioplulamony resuscitation, stabilization, fast Prothrombin time 10-12 sec >100 sec
delivery, Partial thromboplastin 35-50 sec >100 sec
Spotty spinal: 2.5mg diazepam up to 10mg IV Fibrin split products <16 mcg/ml >200 mcg/ml
Fentanyl  1μg/kg  IV Uterine Rupture: Red blood cell fragment No Yes
40% N2O Uterine wall defect resulting in fetal distress or maternal
0.25mg/kg ketamine IV hemorrhage
10-20ml 0.5% lidocaine intraperitoneally Risk Factors: prior C-section, uterine scar, trauma, forces, hard
labor
Most diagnostic sign = fetal distress- loss of fetal heart tones
Continuous  abdominal  pain  &  Hotn        (↑  in  VBAC)
Tx: volume resuscitation & immediate laparotomy & hyster poss
Geriatrics Remifentanil  ↓50-70% Pan, Vec & Roc - ↓20% cerebrovascular dz, & RHF, cardiomegaly, CHF
Geriatrics/Elderly = > 65y.o Ages = >80y.o Succs- slightly reduced dose Extra 0.1 L/min of CO for each additional kilogram of fat.
Progressive loss of functional reserve in ALL organ systems Beta receptor responsiveness 2nd to  ↓  receptor  affinity  &  
1 % decline each year after 30 years old alterations in signal conduction - ↓  cAMP Respiratory:
No Changes: atracurium, neostigmine, Edrophonium Increased: Diaphragm, O2 consumption, CO2 production, WOB,
Homeostasis: Able to maintain; however, less able to restore when RR, Hypoxemia
trauma, disease or drug Anesthetic Considerations: Decreased: ERV, IC, FRC, VC, PaO2, chest wall compliance,
Positioning  and  padding  of  importance  d/t  fragile  skin,  ↓  sub  q   No Change: PFT’s,  ling  compliance
A-A gradient: >/= 20 (nml 8) fat, & poor skin turgor. -- Collage  loss  &  ↓  elasticity- sensitive – Miscellaneous: Right to Left shunt , TV within CC, Restrictive
muscoskeletal limitations- some positioning not possible
Surgical Risk: Hepatic/GI:
[Link] 2. Patient status Preoperative concern: Heart> renal> hepatic > pulm > multi- DM ↑  GERD,  cholelithiasis,  pancreatitis  &  nonalcoholic fatty liver dz
[Link] dz 4. Elective vs. emergent & type of surgery Postoperative concern: Heart & lungs ↑  liver  enzymes  ,  ↑  glucose,  cholesterol
Renal:
Geriatric System Changes CAD & COPD = CXR Increased: GFR renal tubular resorption,
Cardiac: fx declines 50% (20-80 y.o) impaired Na+ excretion = worse HTN
Increased: left  ventricular  wall  thickness,  LVH  d/t  chronic  ↑   IV induction = SLOWER Inhalation Induction= FASTER No change: RBF
afterload, left ventricular wall tension (law of Laplace), afterload,
cardiac workload 2nd to  ↓  aortic  compliance  - AC, SBP, PVR, Postoperative delierum Endocrine:
Circulation time, conduction fibrosis, dysrhythmias, SA node cell *Higher Risk for delirium and Postoperative cognitive Hyperinsulinemia- activates SNS  =  Na  retention  =  ↑  HTN
loss, Vagal tone – d/t  ↓  sensitivity  of  adrenergic  receptors,  systolic   dysfunction
HTN  d/t  ↑  PP  2nd to vessel stiffness, 1-3 days post op- resolves in hours to days Anesthesia Management:
Decreased: cardiac reserve, CO –d/t  ↑  in  AL,  CI,  HR,  left  ventricular   @ risk: > 70 yrs, hx of delirium, etoh abuse, narcotic Neck circumference single best predictor of difficult airway
compliance, chronotropic & inotropic responses, baroreceptor fx, Greatest w/Orthopedic procedures BMI of 50 = RSI w/ cricoid pressure
adrenergic sensitivity Haldol – benzos make worse- unless ETOH related ↑  Brachial  plexus  injury          
No Change: DBP, resting systolic fx, excitation-contraction coupling, Phen-phen use – inquire about valve issues
ionized Ca levels, contractile proteins, SV Geriatric & Regional Appetite suppressant – SSRI’s  =  catecholamine  depletion  
↓  Cmin  for  LA  
Respiratory: Restrictive Regional:
Increased: vocal cord stimulation SAB Epidural ↓  LA dose by 20% 2nd vascular engorgement of the
for closure, airway obstruction, ↑DOA ↓  DOA epidural space, the level and onset of an epidural block can be
risk of aspiration, pulmonary ↑Sensory  block ↓  Motor  Block unpredictable
complications, physiologic dead ↓  Dose ↓  segment  dose
space, WOB, potential for ↑  volume  cephalad  spread Pharmacology:
hypoxia, FRB, Closing volume ↑  Vd  for  meds
and Closing capacity, alveolar T8 for TURPS
compliance, resp depression Cysto SAB @ T10 Drugs distributed mainly to lean tissue dosed on LBW & include:
w/opioids, collagen Thiopental, propofol, rocuronium, vecuronium, atracurium,
PaCO2-PACO2 gradient d/t V/Q mismatch, VD/VT\ 5 Similarities of Neonates to Geriatrics: midazolam cisatracurium, fentanyl, sufentanil, & remifentanil
Decreased: elastin fibers, tissue elasticity, lung recoil, ability to 1.↓  ability  to  ↑  HR  2nd to hypovolemia
cough, chest wall compliance – kyphosis, VC, ERV, IRV, response to 2.↓  arterial  O2 tension Drugs distributed to lean & adipose dosed on TBW & include:
hypoxia & hypercarbia, protective reflexed, cervical spine & TMJ 3. impaired ability to cough Succinylcholine and Dexmedetomidine
mobility, ease of mask ventilation, PaO2 (0.4mmHg/yr. after 20) 4.↓  renal  tubular  function
No Change:PaCO2, PAO2 5.↑  susceptibility  to  hypothermia   Hetastarch- 20ml/kg – based on IBW

CC=FRC @ 44 y.o CC > FRC @ 66yo Progeria OSH (pickwickian) OSA

Closing volume is 10% of VC in the young & 40% in the elderly Aka: Hutchinson-Gilford Syndrome- premature aging Obesity hypoventilation syndrome obstructive sleep apnea
PAO2-PaO2 gradient = 0.21 (age +2.5) Average death 13 y.o = males & females males > females
PaO2 = 102-Age/3 Airway effects: mandibular hypoplasia, micrognathia, glottis awake PaCO2 > 45 mmHg, normal awake PaCO2
opening is narrow doesn't exhibit nocturnal airway sleep induced obstruction
Endocrine: Anesthesia concerns: organ systems fx, positioning obstruction unless concomitant OSA
Increased: Insulin resistance, heat loss pulmonary hypertension
Decreased: heat production, hypothalamic temp regulation Alzheimer’s somnolence, sleep apnea, normal paCO2, pH, pulm
Deposition of amyloid beta peptides produces neuritic plaques hypercapnia, & hypoxemia compliance
GI/Hepatobiliary: & neurofibrillary  tangles=  ↓  NT  fx  &  death of neurons. ↓  alveolar  ventilation, cyanosis
Increased: gastric pH, AAG-1  (↑  binding  of  basic-LA, opioids) The limbic system and cortex are most affected. Polycythemia, enlarged heart,
Decreased: liver mass, HBF, liver fx, biotransformation, albumin Dx:only postmortem examination of brain tissue is definitively Hypoxemia – PaO2 < 65mmHg
production, PCHE – MEN, gastric emptying, plasma clearance diagnostic of Alzheimer's Rales
No change: Hepatocellular fx Risk Factors: Family history, age greater than 65, poor
education, history of SZ, head injury, MI, & hypothyroidism. Liposuction
Nervous System: Tx: Cholinesterase inhibitors: rivastigmine, donepazil, & 1ml of wetting solution per 1ml of fat. >5000 ml – fluid overload
Increased: skeletal muscle atrophy, degeneration of peripheral nerve Galantamine concern may promote- hypoxemia, HTN, & pulm edema
cells, Threshold –proprioceptor, hearing, temp thresh, touch thresh, S/E: nausea, vomiting, bradycardia, syncope, & fatigue. Wetting solution: used to emulsify fat, provide anesthesia, create
vision thresh, CSF, cerebral cortex neuron loss, SNS hemostasis – solution is dilute epi 1:100,000 & lidocaine 0.05-
Decreased: CBF, intracranial volume, gray matter, brain mass, Anesthesia/Pharm: 0.1%
skeletal muscle steadiness-strength-control, conduction velocity, Acetylcholinesterase  inhibitors  may  have  a  ↑  DOA  w/succs PE is # 1 concern = 25% of liposuction deaths
↓response  to  β Anticholinergic – Use glycopyrrolate is blood brain
No change: Autoregulation May be resistance to NDMR d/t use of acetylcholinesterase Positioning
inhibiting drugs Lateral Position
Renal: ↑  risk  of  rhabdo  
Increased: BUN, ADH response to hypertonic saline load (caution Obesity Awake & spont breathing: dependent lung better V & Q
w/fluids), ability to develop hyper/hypo kalemia Values: Anesthetized & spont breathing: non-dep better V, depen- better Q
Decreased: kidney  mass,  RBF  d/t  ↓CO  (50%),  renal  plasma  flow,   BMI < 18.5 = Underweight 18.5-24.9 = Anesthetized    &  mech  vent:↑  non  dep  V,  depen  better  Q  =  ↑V/Q  
GFR, renal fx, muscle mass, creatinine production, fluid handling Normal Most compromised position in anesthetized & mech vent patient
(prone to fluid overload), Na handling, concentrating ability, response 25-29.9 = Overweight 30-39.9 = Obesity
to ADH, response to aldosterone 40-49.9 = Extreme obesity 50-59.9 = Ax roll/chest roll – to protect brachial plexus = relief of pressure
No change: serum creatinine Superobesity 60+ = Super-super obesity from  axillary  neurovascular  bundle  &  prevent  ↓  blood  flow  to  hand
*Creatine Clearance is most sensitive indicator of renal fx in elderly
70ml/min @ y.o >28 BMI or 20% >35 BMI (45%> IBW) morbid Postoperative tonsillectomy patient with head down
Thermoregulation: > 80 shivering @ 350 vs. younger pt. at 36.1C0 obesity
Lithotomy
IBW = ht in cm – 100 (m) or 105 (f) 1cm=2.54 in ↓  FRC  
2
Pharmacology: BMI = kg/m Respiratory embarrassment – Pulm edema, Restrictive lg dz
Increased: circulation time, body fat, Vd for lipids, recovery of VA 5 nerves that may be injured
Decreased: muscle mass, body head production, core body temp, BMI > 35- 40 is cut off for ambulatory surgery center Common Peroneal (most common)
basal metabolic requirements, MAC, Total body water, Vd for water Sciatic saphenous
soluble drugs, dosing for barbs-- opioid antagonists-- benzos Cardiac: Femoral Obturator (excess flexion)
Doses: Increased: CO, Blood Volume (50ml/kg), incidence of HTN
Increase: Atropine, Isoproterenol & other Beta agonists EKG  Δ’s  :  Low  QRS  voltage,  LVH  criteria,  left  atrial   Prone
Decrease: enlargement, t-wave flattening inferior & arterial leads, & Upright to prone = ↓SV, CO, FRC
Thiopental- ↓  15% induction - 2.1mg/kg- / same main prolonged QT Supine  to  prone  =  ↑  FRC
Propofol - ↓  20%  - 1.7 mg/kg Etomidate:    ↓0.  2mg/kg       OSA ♥  effects:  polycythemia, pulmonary & systemic
Midazolam- ↓  50% 0.02-0.03mg/kg Opioids:  ↓  50% vasoconstriction, ↑  risk for ischemic heart dz &
Trendelenberg position Arterial hypoxia 2nd decreased diffusion of O2 across alveoli Goals of anesthetic management of organ donors:
↑  MAP, PCWP, SVR, venous return, CVP, ICP No RSI – awake intubation with head up position= safer *Maintain euvolemia
↓  CI,  oxygen  delivery,  O2 consumption, CO 1. SBP > 100mmHg
↓  TLC,  VC,  FRC   Preoperative Assessment 2. PO2 > 100mmHg
*FRC & pulmonary compliance MOST Mouth opening – 40mm -- 2 fingerbreadths 3. Urine Output > 100ml/hr
West Zone III Thyroidmental distance - > 6.5 cm nml < 6= difficult airway 4. Hbg concentration 100g/L
↑  Pulm  edema Silent MI – HTN & DM 5. CVP 5-10mmHg
ETOH – Hypomagnesium, hypokalemia, metabolic alkalosis 6. FiO2 < 40% (if tolerated)
11 Complications of steep trendelenburg 7. Glucose < 200mg/dl
[Link] 2. Blood loss/hypovolemia Inappropriate for Ambulatory Surgery: 8. Peak airway pressures < 30mmHg
3. VAE 4. Ocular complications 1. Major Surgery/ Major blood loss
5. venous thrombus 6. ETT migration 2. ASA 3& 4 Absolute contraindications: active infection
7. atelectasis 8. Neuropathy 3. Morbidly obese
9. arthralgia 10. Finger injuries 4. Complex pain management Intraoperative renal considerations:
11. regurgitation 5. Fever, wheezing, nasal congestion, cough, URI 1. SBP > 90mmHg 2. MAP > 60mmHg
6. Patients susceptible to MH 3. CVP > 10mmHg
Sitting 7. Uncontrolled sz activity
900 = sitting 450 = beach chair 8. Active substance abuse Liver Transplant
Hotn is most frequent complication 9. Active infection Severe acidosis – THAM – trishydroxymethl
Air embolism most likely with this position 10. Uncooperative or unreliable patients
Least  likely  to  have  ↑  ICP   11. No responsible adult @ home during convalescence Pneumoperitoneum
Neurosurgery 4 reasons to have head up: provides better access, Hemodynamic  Δ’s
improves venous drainage, lowers ICP, easier to observe face Medications to Hold before surgery ↑SVR  &  MAP  ,  ↓  CI          Healthy  patient  – no  Δ  in  CO,  HR
Oral Glycemic – am of surgery 5  pulmonary  fx  Δ’s
Avoid excessive cervical flexion = impedance of arterial & venous Diuretics- am of surgery ↑PIP ↓VC ↓FRC
blood flow—Hypoperfusion of the brain- macroglossia ↑Ppl ↓respiratory  system  compliance
*Maintain at least 2 fingerbreadths between chin & sternum Postoperative complications
Postoperative pulmonary complications: thoracic and upper Eye Surgeries
Lawn  chair  ↓  sciatic  nerve  injuries   Abdominal surgery = highest risk. Normal IOP: 10-22mmHg based on rate of aqueous humor
. formation & rate of aqueous humor outflow
Prone Hypoxia in the PACU: hypoventilation  &  ↑  R  to  L   3 parameters: CVP, arterial blood pressure, arterial partial pressure
Large breast = positioning medial and cephalad intrapulmonary shunting 2nd to  ↓  FRC  (#1) IOP  ↑  with  hypercarbia        IOP  ↓  with  hypocarbia  
Strabismus: cardio effects of ocular meds, oculocardiac reflex,
vision loss during prone procedures in Ischemic optic neuropathy and HoTn 2nd to #1- Hypovolemia HTN 2nd #1 Pain MH, PONV
central retinal artery occlusion account for 89% of cases of N2O-avoid 10days postop after use of sulfur hexafluoride
postoperative vision loss in prone #1 Postoperative Complication – PONV
High risk PONV = children, women, previous hx, hx of OLV
Pneumocephalus motion sickness, anxiety, abd, gyn , laparoscopic, opioids, Vent management: FIO2 @ 1.0, TV 10-12ml/kg, PaCO2 35-40
Caused because air enters the cranium while the pt. is in a head up surgical duration Hypoxia: #1 – check position of DLT w/FOB, CPAP, PEEP
position at a time when the volume of intracranial contents has been CPAP- the single most effective means to increase PaO2 w/OLV
reduced as a result  of  some  combo  of  ↓  CO2, good venous drainage, Carotid Endarterectomy CPAP- non-dependent lung 5-10cm H2O
osmotic diuresis, CSF loss from field. PaCO2 35-45 mmHg – Avoid  ↓  CO2 → vasoconstriction PEEP- dependent lung 5-10cm H2O
Stump pressure transmitted pressure through the circle of willis Other actions: periodically inflate collapsed lung, ligate PA
Manifests: delayed emergence from GA, severe HA < 50 = shunting Greatest risk = hypoxemia
Avoid hyperglycemia ↓  PaO2 2nd to right to left intrapulmonary shunt
Bladder perforation Maintain BP > preop BP (MAP 80-100) Tubes: White- Right, Carlens, Left, Robertshaw- both (no hook)
Awake- shoulder pain Bradycardia d/t surgical baroreceptor stim = lidocaine by surgeon
Anesthetized – tachy, htn or hotn Post-operative HTN = carotid sinus baroreceptors Inhibition of HPV
1. Hypocapnia 2. Vasodilators [Link]
Total parotidectomy Causes of morbidity & mortality #1- MI & #2-Stroke 4. High or low pulmonary artery pressure
spares the facial nerve, while a radical parotidectomy removes the 5. High or low mixed venous partial pressures
facial nerve Heparin 5,000-10,000 & Protamine 0.5mg/100 u of Hep 6. Pulmonary infections
Shunting of the blood away from non-dependent lung in OLV
Hyperextension of neck = compression of ipsilateral and/or Monitoring: EEG, somatosensory evoked potentials, internal
contralateral vertebral arteries carotid artery stump pressure, and transcranial Doppler. During Nasal Intubation
awake carotid endarterectomy, the patient's neurologic status and 1. Temporomandibular surgery
Bone Cement: responsiveness is the indicator of cerebral perfusion 2. Lefort I or II osteotomy for surgical repositing of maxilla
Methylmethacrylate toxicity = sudden hotn 3. I & D of severe oral facial infections
MOA – transient fat/air embolism from bone marrow or causes Nerves: Smile: facial nerve, say "EEE": superior and recurrent 4. Intermaxillary fixation
vasodilatation  &  ↓  SVR   laryngeal nerves, shrug shoulders: spinal accessory nerve,
Minimized  MMA  toxicity:  hydrate  &  ↑  FiO2 swallow: glossopharyngeal, stick his tongue out: hypoglossal TRAM
nerve Avoid vasopressors and N2O during abd closure
Radial Prostectomy- complications
1. Hemorrage (#1) 2. Compromised vent fx Nerve Injury: phrenic, vagus, recurrent and superior laryngeal Mediastinoscopy
3. Air embolism 4. Obturator nerve injury nerves, ansa hypoglossi, and hypoglossal nerves Surgical procedure where a mediastinoscope is inserted into the
5. DVT mediastinal space in order to view and biopsy lymph nodes.
AAA Monitors: Art-line & pulse ox Right BP cuff – Left
8 causes of rhabdomyolysis Prior to clamping- 5000U Heparin IV, PAP 5-12mmHg The most common reason for doing this bronchogenic carcinoma
1. Major crush injury [Link]/electrical injury Above  clamp:  ↑  EDV,  ESV,  SVR,  MAP,  ↓LVEF,  CO Compression: innominate or Right brachiocephalic
3. Acute muscle ischemia d/t arterial occlusion Below  clamp:        ↓SVR,  MAP,  tissue  perfusion Complications: #1- hemorrhage & #2pneumothorax tearing of
4. Acute muscle injury 2nd prolonged immobilization Anaerobic metabolism & lactate accum great vessels, chylothorax,bronchospasm from airway
5. Compartment syndromes [Link] Release of Clamp: ↓SVR,  BP,  CO  2nd volume shifts- central manipulation, air embolism, arrhythmias, & esophageal laceration.
7. Extreme lithotomy 8. Hyperlordotic position hypovolemia  =  ↓  venous  return  
Maintain intravascular volume! Mesenteric Traction Syndrome
6 Congenital syndromes associated with difficult intubation Thoracic artery = 11% spinal cord ischemia & 6% paraplegia Hypotension, tachycardia, cutaneous hyperemia, and hypoxia are
[Link] 2. Goldenhar [Link]-fiel Ventilation: hyperventilate, and CPAP to nondep signs caused by the release of vasoactive amines (principally
4. Pierre Robin 5. Treacher Collins 6. Turner Classified: Debakey & Stanford prostacyclin) from the vascular bed of the mesentery. As a result,
serum prostaglandin levels increase substantially
Ludwig’s  Angina Transplant
Overwhelming generalization septic cellulites of submandibular Organs most frequently transplanted: kidney & liver Tx: H1 & H2, Ketorolac, Neo
region. Usually after dental procedures. S/S: chills, fever, drooling, 6 brainstem reflexes absent in brain death:
ability to open mouth, difficulty speaking. Caused by hemolytic 1. Pupillary response to light Tourniquet
streptococci. 2. Corneal reflex Inflated: Arm 50mmHg > SBP (250mmHg)
Airway management: preliminary tracheotomy using LA in awake 3. Oculocephalic reflex (dolls eyes) Leg 100mmHg > SBP (300mmHg)
patient = Safest 4. Oculovestibular reflex (caloric response) Tourniquet times should not exceed 1.5 to 2 hours
5. Gag & cough reflex ↓CVP  &  SBP  
Contraindications for Cricothyrotomy 6. Facial motor response ↑  HR, ETCO2, PaCO2, serum K, & serum lactate levels
Children < 6 years old
Laryngeal fractures Restrictive Lung Disease
Extrinsic: pectus carinatum, pectus excavatum, kyphosis, scoliosis,
Scleroderma and flail chest as well as obesity, neuromuscular disorders
Severe jaw limitation Intrinsic: Sarcoidosis
Decreased compliance = difficult ventilation
Bowel Obstruction Units & Measurements Prevent hypoxia from lack of oxygen flow, but does not prevent
metoclopramide should never be administered to a patient suffering PO2 = 760mmHg the flow of anesthesia gases (still possibly allow a hypoxic mixture
from a bowel obstruction due to the possibility of perforation from its 1mmHg=1.36cm H2O of gases to be delivered).
prokinetic effects 1atm = 760mmHg=14.7 psi = 101 kPa = 1 bar
1 psi =54 mmHg Pumping Effect:
Nerve Conduction Pathways An intermittent back pressure caused by positive pressure
Paleospinothalamic tract (medial spinothalamic tract) projects to the % = g/100 ml ventilation  or  use  of  the  oxygen  flush  valve  results  in  ↑  vaporizer  
medial thalamic nuclei - associated with autonomic & emotional mcg/ml = 1,000,000/denominator output. (not happening on newer machines)
responses to pain. Concentration= Amount/Volume Low: flows, vapor dial settings, levels of anesthetic in vaporizer
spinocervical tract possesses fibers that ascend to the lateral cervical Amount = concentration x volume High: RR & PIP
nucleus and then cross to the contralateral thalamus.
spinomesencephalic tract projects to the midbrain reticular CO2 Absorber Tipping of the vaporizer = most agent to the patient
formation and may generate nondiscriminatory pain sensations. Baralyme = 80% Ca(OH)2 + 20% Ba(OH)2 (no silica) Breathing Systems:
Neospinothalamic tract (lateral spinothalamic tract) and sends fibers 10.2L of CO2/100g Open System- no mask on the face ie. NC
to the posterior nuclei of the thalamus- location and intensity of pain. Soda Lime = 94% Ca(OH)2 + 5% NaOH + 1% KOH Semi-Open: mask on face- no  rebreathing  =  ↑  FGF  
26L of CO2/100g Semi-Closed: mask on face- some rebreathing w/ regular flows
Burns Forms: CaCO3 + NaOH (2KOH) → neutralization reaction Closed: Mask on Face: - complete rebreathing APL closed & low
Types: Chemical, electrical, thermal, and inhalation CO2 = exothermic flows (150-500ml/min physiological requirements)
Classification: first, second, third, or fourth degree. 4-8 mesh = optimal surface area
First-degree consists of erythema w/ only microscopic damage to the Silica  =  ↑  hardness  &  ↓  dust Mapleson Systems:
superficial epidermis. Exhausted when exposed to carbonic acid – Ethyl Violet Prevention of rebreathing – spont ventilation: A> DFE > CB
Second degree (partial thickness), extend through the epidermis into Prevention of rebreathing Controlled vent: DFE > BC > A
the dermis. Spontaneous regeneration of the skin is possible CO2 absorber: soda lime & carbon dioxide occurs 2 steps. All Mapleson can ventilate the apneic patient
Third-degree: total destruction of the skin, dermal appendages, & #1 CO2 + H2O --> H2CO3 (intermediate product of reaction) Mapleson D modified = Bain → best for controlled vent
epithelial elements occurs with no spontaneous regeneration of #2 H2CO3 + 2NaOH --> Na2CO3 + 2H2O + heat. (final) Mapleson E only one w/o reservoir bag
the skin possible. Mapleson F = Jackson Reese - peds  d/t  ↓  WOB  but    heat  loss
Fourth-degree: involve muscle, fascia, and bone. E cylinder: O2 = 660 Liters, 2200 psi
Forced Air Warmer
Fluids: first 24 hours is % body surface area X Kg X 2 to 4. (hct) Air = 625 Liters, 1800 psi Law of Laplace Maximum temp 48 C
T=P x r Average contact 46 C
Rule of Nines: adults: each arm 9%, each leg 18%, the entire trunk is N2O = 1590 Liters, 750 psi
36%, head 9%, perineum 1%. Blood Salvage Contraindications:
Woods Metal plug melts @ 2000 F (71.4C). and 3000 psig Infection malignant cells
Hct & viscosity: ↑  significantly   Woods Metal = Tin, Cadmium, Lead, Bismuth Urine bowel contents
Electrical: ↑  renal issues maintain UO 1-1.5ml/hr Amniotic fluid
UO: Adults 0.5ml/kg/hr < 30kg peds 1ml/kg/hr When N2O < 745 = no more liquid & ~ 400L of N2O remains
Upper airway inhalation injury: superheated air & steam. Heat & Moisture Exchanger:
The larynx, epiglottis, tongue, and pharyngeal tissue swell rapidly = Equipment Conserves some exhaled water & heat–return to pt. in inspired gas.
complete airway obstruction. DISS- Quick connectors indexed for specific gas- SAFETY & is Bacterial/viral filtration: Hydrophobic > Hydroscopic
a check Valve- Wall Hose to machine – pressor of 40-50psig Contraindicated: copious secretions, uncuffed endotracheal tube
Lower airway inhalation injury: soot and chemical toxins. free floating value on back of gas machine
The toxins produce acidic & alkaline compounds disrupt the capillary at pressure of 1380 kPa (200 psi) or less. LMA
permeability of pulmonary epithelium = alveolar damage. Closes if cylinder pressure is on & pipeline pressure is off Contraindicated:  risk  for  aspiration,  fixed  ↓  pulmonary  
Hanger Yoke- compliance, unable to understand instruction, hiatal hernia
CO: > 15 = toxic tx = 100% O2 Pinks for E cylinders – O2 pin index 2,5 & N2O is 3,5
Diaphragm Valve : 1st & 2nd regulators -fx is to reduce pressure Pacemaker
Anesthesia: OR 28-30 0 C, most heat loss from burns = evaporation 1st stage- 40-50psig (intermediate) Chamber paced A,V,D
Resistant  to  NDMB  d/t  ↑  #  of  cholinergic  nicotinic  receptors   2nd stage- 40-50 to 16 psig Chamber sensed A,V,D
O2 Flush Valve- 35-75L/min, 40-50 psig (intermediate) Response – Inhibit, Trigger, Double, O-none
Trauma Pressure Sensor Shut-Off Valve: (only senses PRESSURE)
Most common cause of coagulopathy = Dilutional thrombocytopenia Senses O2@ 50 psig, shuts of N2O if O2 pressure falls Pulse Oximetry:
Basal skull fx : blood behind ear drum, CSF from nose & ears O2 pressure @ 25psig to keep open Beer Lambert
No  drugs  that  ↑  ICP:  ketamine,  succs,  N2O Needle Valve for waste scavenging: flow (not suction or Fx w/ 2 wavelengths: Red light 660 nm – Deoxygenated Hbg
vacuum) Infrared light 940nm- Oxygenate Hbg
Cardiogenic Shock vs. Hypovolemic shock_____ Fingers are one of the last places to showing desat (central first)
↑  PAOP  >  15mmHg,  ↓CI,  ↑  SVR            ↓  PAOP,  nml  CI,  nml  or  ↑  SVR Gas flow during breathing:
Inspiration: inhalation check valve & soda lime, through soda Changes in Pulse Oximetry
Autonomic Hyperreflexia lime- to CGO and from rebreathing bag False High: Caboxyhemoglobin & methemoglobin, severe anemia
65-80%  ↑  T7  (unlikely  below  T10) Expiration: though exhalation check valve to APL/rebreathing SpO2 < 85%
Triggering stimuli: bladder, or bowel distention, heat/cold, uterine bag False Low: Methylene blue, prominent venous pulsations, injection
contractions, pyelonephritis if dyes- indigo carmine, lymphazurin, nitrobenzene, indocyamine
S/S: Hallmark – HTN & reflex bradycarda Components of the High Pressure system of AM : > 55psig green, patent blue
Below level of injury – SNS activation = vasoconstriction & HTN [Link] yoke
Above level of injury- SNS blockade = vasodilatation 2. yoke block w/ check valves (free floating) Capnography:
3. cylinder pressure gauge
Pain- Neurolytic blocks 4. cylinder pressure regulators
Indicated for cancer patients with incurable, intractable cancer pain
Not permanent- may last 2-6 months Components of intermediate pressure system of AM: 40-50
Celiac plexus block for pancreatic cancer = most effective psig
Blocked with alcohol or phenol 1. Ventilator power inlet
Most common: celiac plexus, lumbar sympathetic chain, hypogastic 2. pipeline inlets, check valves, pressure gauges
plexus and ganglion impar 3. flow meter valves 5 monitors that can detect disconnection
Greater occipital nerve block = relief from cluster headaches 4. oxygen pressure- failure devices [Link] oximetry
5. oxygen second stage regulators 2. mass spectrometer
Pain fibers from the head are carried within the trigeminal, 6. flush valve 3. capnography
facial, glossopharyngeal, and vagus nerves. 4. stethoscope
Components of the low-pressure system of AM: 16 psig 5. spirometer
Corticosteroids are the most common multipurpose coanalgesic used 1. flow meter tube
for cancer pain 2. vaporizers Mass Spectrophy:
3. check valves Gases analyzed: CO2, O2, N2 & inhaled agents (Not PaO2)
Post-operative shivering medications: 4. CGO Gas sampled is ionized by an electron beam and passed through a
1. Clonidine magnetic field.
2. Physostigmine Tec 6 vaporizer – dual circuit, gas vapor blender
3. Serotonin antagonists 390 C & pressurized to 2 atmospheres (1300mmHg) Raman: measures gas concentrations by analyzing the intensity of
4. Propofol. @ high elevation – need  to  ↑  concentration  to  raise  PP   light emitted when a gas sample returns to an unexcited state after
being energized by a laser beam
Electricity: Oxygen supply failure alarm
Macroshock = large voltage applied to skin/tissue Sets off an alarm if the oxygen pressure falls below a standard set Infrared: they detect gases based on the amount of infrared light
Microshock  =  small  voltage/current  directly  to  the  ♥ by the manufacturer typically 30 psig that is absorbed by the sample- can not detect oxygen content
V-fib caused by 50microamp-micro/100-2500 milliamp- macro Must engage within 5 seconds of the disconnect and cannot be Most popular in the OR & based on beer lambert
disabled by the anesthetist
Grounded in OR: Power supply, Patient, The floor Isoproterenol = high false measurements
Peripheral Nerve Stimulator -- CURRENT Gas Laws Law of Laplace
TOF – 2Hz – two twitches per second or one every 0.5 seconds “Can These Girls Possibly Be Virgins” T= P x r – cylindrically shaped structures thus ↑T  =  ↑  r    
Tetany- 5 seconds @ 50Hz Applies to: blood vessels, left ventricle (Frank-Starling)
DBS-2 trains of 3 impulses @ 50Hz – separated by 750 ms (best to B T= (P x r) /2 -- spherically- shaped structures thus  ↑r  =  ↑  T,  ↓r  =  ↑
determine fade) Boyle = P1V1 = P2V2 P
Post Tetanic- 50 Hz x 5 seconds – 3 second pause – stim @ 1 Hz Applies to alveoli – ARDS
# of visible post tetanic twitches correlates inversely to time P V Charles = V1/T1 = V2/T2
required for return of single twin or train-of-four responses Humidification
Ulnar nerve = adductor pollicis- abdomen Gay-Lussac = P1/T1 = P2/T2 Relative Humidity (%) = actual vapor pressure x 100
Facial nerve = orbicularis oculi – laryngx (Temp on bottom) Saturated vapor pressure
Twitches:
1. one visible twitch = 95% blockade G C ↓  T  =  ↓  capacity  to  hold  H2O → H2O condenses
2. two visible twitch= 80-85% blockade T
3. three visible twitches= 75-80% Partial pressure of saturated water vapor @ 370 = 47mmHg
4. four visible twitches = < 75%
Avogadro’s  Hypothesis = 1 mole of gas @ STP = 22.4 Liters Ohms Law
BIS – based on HYPNOSIS STP = C and 1 atm SVR
100- Awake Avogadro’s Number
90-70- Light/Moderate Sedation 6.023 X 1023 = 1 mole
70-60- Deep sedation (low probablility of recall) 1 mole = 00 = 1 atm = 760 mmHg = 22.4L
60-40- general anesthesia Gases liquefy if: (1) sufficient pressure is applied and Ostwald Solubility Coefficient
40-10- deep hypnotic state (2) temperature is below critical temperature Solubility of a gas in a fluid
10-0- flat line EEG N2O = 39.5 0C Amount of gas in solution is inversely proportion to temp
< 40 reflect burst suppression. O2 = -119 0C Hypothermia  =  ↑  solubility  of  VA  in  blood  &  tissue

Artifact can be produced by: Output from cardiac pacemakers, muscle Fick Diffusion: _____(P1 –P2) (Area) (Solubility)________ Van Der Wals:
activity such as twitching, shivering, or blinking, incorrect electrode (Membrane thickness) ( Molecular Weight) Non-ideal gas behavior
placement, & high frequency electrical devices such as IV pumps and
warming devices can all produce artifact. ***the concentration gradient is the most important factor in Inverse Square Law
determining the rate of diffusion of a drug across a membrane Distance from source = amount of exposure
Paradoxical delta waves may occasionally be seen during anesthetic
maintenance and emergence. % Concentration = (Partial Pressure/Atm) X 100
Three Steps of QA programs:
Blood Pressure Cuffs: 40% of arms circumference Partial Pressure = % Concentration X Atm 1. Define the norm
Overestimation if cuff: too loose, too small, or positioned below the 100 2. Are adverse events caused by deviations from norm?
level of the heart 3. Prevent adverse events
Partial Pressure H2O @ 370 C = 47 mm Hg
Pacemakers ~Concentration effect Fires in OR:
Most  common  indications  =  SSS  &  complete  ♥  block ~2nd gas effect Components needed for Fire: fuel, oxygen & ignition source
Identification codes ~Diffusion hypoxia Steps if fire occurs:
1st = chamber paced ~N2O  =  ↑  V  or  ↑  P  in  gas  spaces   1. Stop ventilation
2nd= chamber sensed -- eletrocautery affects 2. Stop O2 Flow
3rd= response to sensing Laminar Flow: Poiseuilles 3. Extubate patient
4th= programmability rate modulation AICD F=πr4ΔP/8nl Flow 4. Extinguish the fire
5th antitachyarrythmic fx F= flow, r = radius, n= viscosity, l= length 5. Mask ventilate
Doubling the radius = 16x the flow 6. Reintubate
Medications Tripling the radius = 81x the flow
Atropine – 0.5-1mg x3 Isoproterenol ***Δ  in  radius  =  most  dramatic  effect  on  flow History of Anestehsia:
Succs can inhibit the pulse generator d/t fasiculations Angle < 25 degrees = laminar flow Agatha Hodgins→ formed the AANA in 1931
Avoid nitrous if implanted within 1-2 days ago Alice Magaw → 'Mother of Anesthesia
Reynolds #- turbulent flow Cocaine → first LA
Magnet Re= v x d x e/ n Sister  M.  Bernard→ first nurse anesthetist in Erie, PA
Pacer- converts to a fixed rate (asynchronous) mode v = fluid velocity, d= diameter, p=density, n = viscosity
AICD- disables it – loud continuous high pitch sound >1,500-2000 = turbulent flow Legal:
***Density (p) determines flow when turbulent flow present A writ of mandamus= an order by a court to force a party to
Sterilization commence some required action.
Disinfection: destroys most microorganisms- except SPORES Venturi/Bernoulli
Sterilization: all viable forms of microbial life – yes to spores Flow  through  constricted  region  of  the  tube  =  ↑  Flow & Stare decisis= refers to the doctrine of common law in which
7 chemical disinfectants: quaternary ammonium, alcohols, corresponding  ↓  in  pressure  in  area of narrowing courts adhere to the prior decisions of other courts.
glutaraldehydes (Cidex), hydrogen-peroxide, formaldehyde, phenolic Venturi O2 mask, nebulizer, jet ventilation
compounds, chlorine ( bleach) Anterior Leaflet in IHSS Res ipsa loquitor= (the thing speaks for itself) refers to an event
Ethylene oxide- for  objects  that  can’t  be  heated  in  steam  autoclave that would not have occurred 'but for actions of the defendant'.
Glutaraldehyde (Cidex) & hydrogen peroxide = SPORES destruct LeChatelier’s: Law of mass action
Quaternary ammoniums – WILL NOT kill m tuberculosis ↑ concentration of reactant→ reaction to  ↑  products Tort = Civil Wrongdoing
↓ concentration of reactant→ reaction to ↑  reactant (↓  products)
Lasers Negligence = Failure to use reasonable care, which is that level of
Monochromatic (a single wavelength),coherent (it oscillates in the Henry’s  Law care recognized as acceptable and appropriate given the
same phase),collimated (it is a narrow, parallel beam of light). Calculation of dissolved O2 & CO2 in blood circumstances.
Lasers can be both long (CO2laser) and short (YAG laser) O2 – 0.003ml/100ml blood/ mmHg
wavelengths. O2= % FiO2 x5 = PaO2 Replevin= is a lawsuit to recover goods improperly taken by
Regulates the manufacture & marketing of medical lasers FDA CO2 – 0.067 ml/100ml blood/ mmHg another.

Major risks: Thermal injury, eye injuries, electrical hazards, fire, Dalton’s  Law  of  Partial  Pressure Battery= intentionally causing harmful or offensive contact with a
transmission of viruses, and contaminants in the smoke plume Total pressure in a mixture is = to the sum of pressures of each person or to something close to them
gas Assault= intentionally causing the apprehension of an immediate
Nd-YAG laser – OD(optical density) 5 or > for 1,064 nm/Green Ptotal = P1 + P2 + P3  ……..  PN and harmful contact
O2 – 160 mmHg (21%)
N-95 respirator mask: Laser vaporization of condylomatous lesions N2 – 600 mmHg (79%) Four Elements of Malpractice:
d/t release toxic chemicals: benzene & formaldehyde as well as viable Total – 760 mmHg [Link]- prove defendant had a duty to the plaintiff
viruses capable of transmitting the disease [Link] of Duty- prove defendant failed to fulfill duty to defedant
Joule-Thompson 3. Causation - reasonably close relationship proven to exist
ETT: PVC most susceptible to ignition by CO2 lasers A cylinder cools and condenses after opening a valve – Joule is between breach of duty by defendant and the injury that resulted
Red Rubber – wrapped with metallic tape – deflect beam cool [Link] - prove some injury occurred due to the breach in duty
Silicone- if hit with laser- vaporizes & can aspirate parts
Inflate with sterile saline & methylene blue Beer Law Informed Consent Includes:
The intensity of light is altered as transmitted through liquid. 1. Risks
The intensity of the light falls exponentially as light passes 2. Benefits
through the liquid. 3. Complications
~Pulse oximetry & Infrared absorption spectroscopy 4. Alternatives
Infrared → oxygenated Hbg = wavelength 940 nanometers
Visible red→ deoxygenated → wavelength 660 nanometers
Standard Agencies
Department of Transportation: defines compressed gas standard
Interstate Commerce Commission: sets specification for
compressed gas cylinder construction
Federal Food, Drug & Cosmetic Act: defines compressed gas
standard
United States Pharmacopeia: develops purity standards for gases
National Fire Prevention Association: recommendations for the
construction and location of BULK oxygen containers
Compressed Gas Association: sets standards of practice
American National Standards Institute (ANSI): performance &
safety requirements for components of the AM, ETT,
connectors,vacuum & gas pressure regulators
Food and Drug Administration: promulgates standards for medical
devices and gases
Joint Commission: voluntary accrediting agency
American Society for Testing Materials (ASTM): assess
technology & revises standards
National Institute of Occupational Safety & Health: standards to
protect the health & safety of workers

Type I error When researchers, on the basis of a statistical test,

erroneously concludethat there is evidence of an association between
two variables when, in fact, there is not
Type II error When researchers, on the basis of a statistical test,
erroneously conclude that there is evidence of no association between
two variables when, in fact there is