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Notes for Differences in Anesthesia

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Dr. Ravikiran H M Gowda
Dr. Ravikiran H M Gowda

Notes for differences in anesthesia. Description of various topics of anesthesia in the form of differences.

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1 NOTES FOR DIFFERENCES IN ANAESTHESIA DR. RAVIKIRAN H M 2020 Ravikiran JAI JAWAN JAI KISAN
2 GURU KRUPA DR. RAVIKIRAN H M DNB POST GRADUATE STUDENT DEPARTMENT OF ANAESTHESIOLOGY KIDWAI MEMORIAL INSTITUTE OF ONCOLOGY BENGALOORU, KARNATAKA. WITH BLESSINGS OF MY GRANDPARENTS INSPIRED BY: DR. THAMEEM SAIF THANKS TO: MY FAMILY, SENIORS, FRIENDS & DEPARTMENT OF ANAESTHESIA, KIDWAI MEMORIAL INSTITUTE OF ONCOLOGY. Gmail: ravikiranhmkimmi@gmail.com
INDEX SL. NO TOPIC PAGE RESPIRATORY SYSTEM 1. ODC vs CDC 12 2. CXR PA vs AP view 14 3. Respiratory failure types 15 4. Pulmonary edema: cardiogenic vs non cardiogenic 19 5. ARDS vs CHF vs Pneumonia 21 6. ARDS H vs L 22 7. Obstructive vs restrictive lung diseases PFT 23 8. Chronic bronchitis vs Emphysema 24 9. Chronic bronchitis vs small airways disease vs bronchiectasis 25 10. Lobar pneumonia vs Bronchopneumonia vs Interstitial pneumonia 26 11. DLT, Bronchial blockers: Advantage vs Disadvantages 27 12. Bronchial blockers 28 CVS 13. NTG vs SNP 30 14. Cardiac tamponade vs constrictive pericarditis 32 15. Constrictive pericarditis vs restrictive cardiomyopathy 33 16. Inotropes: Dopamine vs Dobutamine vs Adrenaline vs Noradrenaline 34 17. Meph vs Phenylephrine vs Ephidrine 41 18. Racemic adrenaline vs L adrenaline 43 19. Calcium gluconate vs calcium chloride 44 20. Type I vs Type II MI 45 21. Myocardial stunning vs myocardial hibernation vs infraction 46 22. Alpha stat vs pH stat 47 23. Aortic clamping vs unclamping 49 CNS AND NMJ 24. Mature vs immature Ach receptor 52 25. Pattern of neuromuscular stimulation 54 26. TOF vs double burst 55 27. BIS vs Entropy 56 28. Non depolarizing muscle relaxants: steroidal vs benzylisoquinolium vs Ether vs alkaloid 57 29. Scholine phase I vs phase II block 58 30. Atracurium vs Cis-atracurium 61 31. Neostigmine versus sugammadex 63 32. Myasthenia gravis vs Eaton-Lambert syndrome (Myasthenia syndrome) 65 33. Myasthenic crisis vs cholinergic crisis 67 34. Mannitol vs Hypertonic saline 68 35. Phenytoin vs Fosphenytoin 70 36. Head injury: SIADH vs Cerebral salt wasting vs diabetic inspidus 71 37. Carotid endarterectomy : GA vs RA, Premedication advantages vs disadvantages 72 38. CVA: THROMBOTIC vs EMBOLIC vs HEMORRHAGIC 73 HEPATICS 39. Types of Jaundice 74 40. HRS1 & 2 76 41. Hypoxia in cirrhosis: Portopulmonary HTN vs HPS vs cirrhotic hydrothorax 77 RENAL 42. Acute renal failure: Prerenal, renal vs post renal 78 43. RTA1, 2,3 & 4 79 44. Bartter vs Gitelman vs Liddle vs Conns 80 45. Hemodialysis vs hemoperfusion vs hemofiltration 81
4 46. IHD vs CRRT 83 47. Loop diuretics vs Thiazides vs Potassium sparing diuretics 84 48. Nephritic vs Nephrotic syndrome 86 49. Dailysis dementia vs Dialysis disequilibrium syndrome 87 ENDOCRINE 50. Type I DM vs Type II DM 88 51. Type I DM vs MODY 88 52. Dawns vs Somogyi phenomena 89 53. Tight vs classic non tight glycemic control of glucose 90 54. DKA vs HHS 92 55. Hyperthyroidism vs hypothyroidism clinical features 93 56. Thyroiditis:Hashimoto vs DeQueverians vs Reidles 94 HEMATOLOGY 57. Vit K antagonist versus Newer oral anticoagulants 95 58. Heparin vs low moleculae weight heparin vs Fondaparinaux 97 59. HIT 1 & 2 98 60. FFP, Cryo, Fibrinogen concentrate, PCC 99 61. Tranexamic acid vs EACA 100 62. Synthetic blood vs allogenic blood 101 63. Perflurocarbons vs Hb based oxygen carriers 102 64. Hemolytic transfusion reaction: acute vs delayed 104 65. TRALI vs TACO 105 OBSTRETICS 66. Jaundice in pregnancy: ICP vs HELLP vs AFLP 106 67. Thrombocytopenia with AKI D/D in pregnancy 107 68. Thrombocytopenia D/D in pregnancy 108 69. Choice of anaesthesia in PIH: GA vs RA 109 PEDIATRICS 70. Pediatric inhalational vs IV induction 110 71. Pediatric vs adult airway 112 72. Preterm vs term neonate 116 73. Children vs adults regional anesthesia 118 74. Uncuffed vs Cuffed ETT 121 75. Acute Epiglottitis vs Laryngotracheobronchitis 122 76. Omphalocele vs Gastroschisis 123 ENT & OPHTHALMOLOGY 77. Bronchoscope: Storz vs Negus 124 78. Foreign body airway removal: spontaneous vs controlled breathing 125 79. Retrobulbar vs Peribulbar block 126 BARIATRICS & ORTHOPEDICS 80. OSA vs OHS 128 81. Rheumatoid arthritis vs osteoarthritis 129 82. Ankylosing spondylitis vs ankylosis hyperostosis 131 83. Gout vs pseudo gout 132 GENERAL ANAESTHESIA 84. First order vs Zero order 133 85. Potency vs Efficacy 134 86. Types of hypersensitivity 135 87. Stages of Anesthesia 137 88. CO2 absorbents 138 89. Proseal versus I gel 139 90. Red rubber ETT vs PVC ETT 140 91. Pressurzing effect vs Pumping effect 141
92. Midazolam vs Remimazolam 142 93. Midazolam vs Lorazepam vs Diazepam vs Alprazolam 143 94. Barbiturates vs Benzodiazepines 145 95. N2O advantage vs disadvantage 146 96. N2O vs Xenon 148 97. Concentration vs second gas effect 150 98. Thiopentone vs Propofol vs Etomidate vs Ketamine 151 99. Halothane vs Isoflurane vs Sevoflurane vs Desflurane 157 100. Halothane hepatitis type 1 vs type2 161 101. Azeotrope: Halothane/Ether 162 102. Fentanyl vs Ramifentanil 163 103. Propofol vs Fospropofol 164 104. Crystalloids vs Colloids 165 105. NS vs RL 166 106. Colloids: Albumin, Dextran, Gelofusine, Hetastarch, Pentastarch 168 107. Clonidine vs Dexmedatomedine 170 108. Volume control vs pressure control vs pressure support 172 109. Flow trigger versus pressure trigger 174 110. Anaesthesia machine vs anaesthesia work station 175 111. Anesthesia & ICU ventilator 176 112. Yoke block vs yoke plug 177 113. NIST vs DISS 177 114. Direct vs indirect valves 178 115. Atropine, Glycopyrrolate & Hyoscine 179 116. Modified RSI: scholine vs Rocuronium 181 117. RSI: Modified RSI vs Protected RSI 182 118. Priming vs Precurarisation vs self taming 183 119. Serotonin syndrome vs Anticholinergic syndrome vs neuroleptic malignant hyperthermia vs malignant hyperthermia vs thyroid storm 185 120. MH vs AIR 187 121. Familial periodic paralysis hyperkalemic vs hypokalemic 189 122. Airway catheters: Bougie, Guides, AEC, Aintree, stylet 190 123. Respiratory complications during laparoscopy D/D 193 REGIONAL ANAESTHESIA 124. High frequency vs low frequency probe 194 125. Nerve locator vs peripheral nerve stimulator 195 126. Lignocaine, Bupivacaine, Levobupivacaine, Ropivacaine 196 127. Subdural vs Subarachanoid block 199 128. Epidural morphine versus fentanyl 200 129. Interpleural vs paravertebral block 201 130. RLB vs ESPB vs PVB vs TEA 204 ICU and CRITICAL CARE 131. HME filter Hygroscopic vs Hydrophobic 205 132. PEEP vs CPAP 206 133. Nasal cannula vs HFNO 207 134. Surgical tracheostomy vs Percut dilational tracheostomy 208 135. Antibiotics: time dependent vs concentration dependent 209 136. RBC cholinesterase versus pseudocholinesterase in OPCP 210 137. Cardioversion vs Defibrillation 211 138. Monophasic vs Biphasic 212 139. DPL vs E-FAST vs CT in abdominal trauma 213 PAIN & PALLIATION 140. Acute pain vs chronic pain 214
6 141. Nociceptive vs neuropthic pain 215 142. Slow pain vs fast pain 217 143. Somatic vs visceral pain 218 144. CRPS 1 vs CRPS 2 219 145. Neuralgia vs CRPS 220 146. Pain assessment : unidimensional vs multidimensional scales 221 147. Opioids : pure agonist vs mixed agonist/antagonist 222 148. Opioid induced Hyperalgsia: D/D 223 149. Tramadol vs tapentadol 224 150. Palliative care vs Hospice care 225 151. Head ache: Migrane vs Tension vs Cluster 227 152. Headache: Trigeminovascular cephalgias 228 153. Cryoneurolysis vs Peripheral nerve stimulation 229 154. Articular vs Nonarticular pain 230 STATISTICS 155. Standard deviation vs Variance vs coefficient of variation 231 156. Standard deviation vs Standard error 233 157. Sampling vs non-sampling errors 234 158. Point estimate vs confidence interval 235 159. Frequentist vs Bayesian statistics 236 160. Parametric vs non-parametric tests of significance 237 161. Sensitivity vs specificity 238 162. Cohort vs case control vs cross sectional study 239 163. Odds ratio vs likelihood ratio 241 164. Incidence vs Prevalence 242 165. Correlation vs regression analysis 243
Contents ODC vs CDC...................................................................................................................................................................12 CXR PA vs AP view......................................................................................................................................................... 14 Respiratory failure types...............................................................................................................................................15 Pulmonary edema: cardiogenic vs non cardiogenic......................................................................................................19 ARDS vs CHF vs Pneumonia ..........................................................................................................................................21 ARDS H vs L...................................................................................................................................................................22 Obstructive vs restrictive lung ......................................................................................................................................23 Chronic bronchitis vs Emphysema................................................................................................................................ 24 CHRONIC BRONCHITIS vs SMALL AIRWAYS DISEASE vs ASTHMA vs BRONCHIECTASIS.................................................25 Lobar Pneumonia Vs Bronchopneumonia Vs Interstitial Pneumonia ..........................................................................26 DLT, Bronchial blockers: Advantage vs Disadvantages .................................................................................................27 Bronchial blockers ........................................................................................................................................................ 28 NTG vs SNP ...................................................................................................................................................................30 Cardiac tamponade vs constrictive pericarditis ............................................................................................................32 Constrictive pericarditis vs restrictive cardiomyopathy................................................................................................ 33 Inotropes: Dopamine vs Dobutamine vs Adrenaline vs Noradrenaline ........................................................................34 Meph vs Phenylephrine vs Ephidrine............................................................................................................................ 41 Racemic adrenaline vs L adrenaline.............................................................................................................................. 43 Calcium gluconate vs calcium chloride ......................................................................................................................... 44 Type I vs Type II MI ....................................................................................................................................................... 45 Myocardial stunning vs myocardial hibernation vs infraction ......................................................................................46 Alpha stat vs pH stat.....................................................................................................................................................47 Aortic clamping vs unclamping.....................................................................................................................................49 Mature vs immature Ach receptor ............................................................................................................................... 52 Pattern of neuromuscular stimulation.......................................................................................................................... 54 TOF vs double burst......................................................................................................................................................55 BIS vs Entropy ............................................................................................................................................................... 56 Non depolarizing muscle relaxants: steroidal vs benzylisoquinolium vs Ether vs alkaloid............................................57 Scholine phase I vs phase II block .................................................................................................................................58 Atracurium vs Cis-atracurium .......................................................................................................................................61 Neostigmine versus sugammadex ................................................................................................................................ 63 Myasthenia gravis vs Eaton-Lambert syndrome (Myasthenia syndrome) ....................................................................65 Myasthenic crisis vs cholinergic crisis ........................................................................................................................... 67 Mannitol vs Hypertonic saline ......................................................................................................................................68 Phenytoin vs Fosphenytoin...........................................................................................................................................70 Head injury: SIADH vs Cerebral salt wasting vs diabetic inspidus .................................................................................71 Carotid endarterectomy : GA vs RA, Premedication advantages vs disadvantages ......................................................72
8 CVA: THROMBOTIC vs EMBOLIC vs HEMORRHAGIC .....................................................................................................73 Types of Jaundice.......................................................................................................................................................... 74 HRS1 & 2.......................................................................................................................................................................76 Hypoxia in cirrhosis: Portopulmonary HTN vs HPS vs cirrhotic hydrothorax ................................................................ 77 Acute renal failure: Prerenal, renal vs post renal..........................................................................................................78 RTA1, 2,3 & 4................................................................................................................................................................ 79 Bartter vs Gitelman vs Liddle vs Conns ......................................................................................................................... 80 Hemodialysis vs hemoperfusion vs hemofiltration.......................................................................................................81 IHD vs CRRT ..................................................................................................................................................................83 Loop diuretics vs Thiazides ...........................................................................................................................................84 Nephritic vs Nephrotic syndrome.................................................................................................................................86 Dailysis dementia vs Dialysis disequilibrium syndrome ................................................................................................ 87 Type I vs Type II diabetes..............................................................................................................................................88 Type I vs MODY............................................................................................................................................................. 88 Dawn’s vs Somogyi phenomena ...................................................................................................................................89 Tight vs classic non tight glycemic control of glucose...................................................................................................90 DKA vs HHS ...................................................................................................................................................................92 Hyperthyroidism vs hyperthyroidism clinical features..................................................................................................93 Thyroiditis:Hashimoto vs DeQueverians vs Reidles ......................................................................................................94 Vit K antagonist versus newer oral anticoagulants.......................................................................................................95 Heparin vs low moleculae weight heparin vs Fondaparinaux....................................................................................... 97 HIT 1 & 2 Heparin induced thrombocytopenia .............................................................................................................98 FFP, Cryo, Fibrinigen concentrate, PCC......................................................................................................................... 99 Tranexamic acid vs EACA ............................................................................................................................................100 Synthetic blood vs allogenic blood .............................................................................................................................101 Perflurocarbons vs Hb based oxygen carriers.............................................................................................................102 Hemolytic transfusion reaction: acute vs delayed......................................................................................................104 TRALI vs TACO.............................................................................................................................................................105 Jaundice in pregnancy: ICP vs HELLP vs AFLP..............................................................................................................106 Thrombocytopenia + AKI in pregnancy D/D................................................................................................................107 Thrombocytopenia in preganancy D/d .......................................................................................................................108 Choice of anaesthesia in PIH: GA vs RA.......................................................................................................................109 Pediatric inhalational vs IV induction..........................................................................................................................110 Pediatric vs adult airway.............................................................................................................................................112 Preterm vs term neonate ...........................................................................................................................................116 Children and adults and implications for regional blocks ...........................................................................................118 UNCUFFED vs CUFFED ETT..........................................................................................................................................121
Acute Epiglottitis vs Laryngotracheobronchitis..........................................................................................................122 Omphalocele vs Gastroschisis.....................................................................................................................................123 Bronchoscope: Storz vs Negus....................................................................................................................................124 Foreign body airway removal: spontaneous vs controlled breathing.........................................................................125 Retrobulbar vs Peribulbar block .................................................................................................................................126 OSA vs OHS.................................................................................................................................................................128 Rheumatoid arthritis vs osteoarthritis........................................................................................................................129 Ankylosing spondylitis vs Ankylosis hyperostosis .......................................................................................................131 Gout vs pseudogout....................................................................................................................................................132 First order vs Zero order kinetics ................................................................................................................................133 Potency vs Efficacy......................................................................................................................................................134 Types of hypersensitivity ............................................................................................................................................135 Stages of Anesthesia: Guedal......................................................................................................................................137 CO2 absorbents ..........................................................................................................................................................138 Proseal versus I gel .....................................................................................................................................................139 Red rubber ETT vs PVC ETT .........................................................................................................................................140 Pressurzing effect vs Pumping effect..........................................................................................................................141 Midazolam vs Remimazolam ......................................................................................................................................142 Midazolam vs Lorazepam vs Diazepam vs Alprazolam ...............................................................................................143 Barbiturates vs Benzodiazepines ................................................................................................................................145 N2O advantage vs disadvantage.................................................................................................................................146 N2O vs Xenon .............................................................................................................................................................148 Concentration vs second gas effect ............................................................................................................................150 Thiopentone vs Propofol vs Etomidate vs Ketamine ..................................................................................................151 Halothane vs Isoflurane vs Sevoflurane vs Desflurane ...............................................................................................157 Halothane hepatitis type 1 vs type2 ...........................................................................................................................161 Azeotrope: Halothane/Ether......................................................................................................................................162 Fentanyl vs Ramifentanil ............................................................................................................................................163 Propofol vs Fospropofol..............................................................................................................................................164 Crystalloids vs Colloids................................................................................................................................................165 NS vs RL ......................................................................................................................................................................166 Colloids: Albumin, Dextran, Gelofusine, Hetastarch, Pentastarch ..............................................................................168 Clonidine vs Dexmedatomedine.................................................................................................................................170 Volume control vs pressure control vs pressure support ...........................................................................................172 Flow trigger versus pressure trigger ...........................................................................................................................174 Anaesthesia machine vs anaesthesia work station.....................................................................................................175 Anesthesia & ICU ventilator........................................................................................................................................176 Yoke block vs yoke plug ..............................................................................................................................................177
10 NIST vs DISS ................................................................................................................................................................177 Direct vs indirect valves .............................................................................................................................................178 Atropine, Glycopyrrolate & Hyoscine .........................................................................................................................179 Modified RSI: scholine vs Rocuronium........................................................................................................................181 RSI: Modified RSI vs Protected RSI..............................................................................................................................182 Priming vs Precurarisation vs self taming ...................................................................................................................183 Serotonin syndrome vs Anticholinergic syndrome vs neuroleptic malignant hyperthermia vs malignant hyperthermia vs thyroid storm..........................................................................................................................................................185 MH vs AIR ...................................................................................................................................................................187 Familial periodic paralysis hyperkalemic vs hypokalemic...........................................................................................189 Airway catheters: Bougie, Guides, AEC, Aintree, Stylet ..............................................................................................190 Respiratory complications during laparoscopy D/D....................................................................................................193 High frequency vs low frequency probe .....................................................................................................................194 Nerve locator vs peripheral nerve stimulator.............................................................................................................195 Lignocaine, Bupivacaine, Levobupivacaine, Ropivacaine............................................................................................196 Subdural vs Subarachanoid block ...............................................................................................................................199 Epidural morphine versus fentanyl.............................................................................................................................200 Interpleural vs paravertebral block.............................................................................................................................201 RLB vs ESPB vs PVB vs TEA ..........................................................................................................................................204 HME filter Hygroscopic vs Hydrophobic .....................................................................................................................205 PEEP vs CPAP ..............................................................................................................................................................206 Nasal cannula vs HFNO...............................................................................................................................................207 Surgical tracheostomy vs Percut dilational tracheostomy..........................................................................................208 Antibiotics: time dependent vs concentration dependent .........................................................................................209 RBC cholinesterase versus pseudocholinesterase in OPCP.........................................................................................210 Cardioversion vs Defibrillation....................................................................................................................................211 Monophasic vs Biphasic..............................................................................................................................................212 DPL vs E-FAST vs CT in abdominal trauma ..................................................................................................................213 Acute pain vs chronic pain..........................................................................................................................................214 Nociceptive vs neuropthic pain ..................................................................................................................................215 Slow pain vs fast pain .................................................................................................................................................217 Somatic vs visceral pain ..............................................................................................................................................218 CRPS 1 vs CRPS 2.........................................................................................................................................................219 Neuralgia vs CRPS .......................................................................................................................................................220 Pain assessment : unidimensional vs multidimensional scales...................................................................................221 Opioids : pure agonist vs mixed agonist/antagonist...................................................................................................222 Opioid induced Hyperalgsia: D/D................................................................................................................................223
Tramadol vs tapentadol..............................................................................................................................................224 Palliative care vs Hospice care....................................................................................................................................225 Head ache: Migrane vs Tension vs Cluster..................................................................................................................227 Headache: Trigeminovascular cephalgias ...................................................................................................................228 Cryoneurolysis vs Peripheral nerve stimulation..........................................................................................................229 Articular vs Nonarticular pain .....................................................................................................................................230 Standard deviation vs Variance vs coefficient of variation .........................................................................................231 Standard deviation vs Standard error.........................................................................................................................233 Sampling vs non-sampling errors................................................................................................................................234 Point estimate vs confidence interval.........................................................................................................................235 Frequentist vs Bayesian statistics ...............................................................................................................................236 Parametric vs non-parametric tests of significance....................................................................................................237 Sensitivity vs specificity ..............................................................................................................................................238 Cohort vs case control vs cross sectional study ..........................................................................................................239 Odds ratio vs likelihood ratio......................................................................................................................................241 Incidence vs Prevalence..............................................................................................................................................242 Correlation vs regression analysis...............................................................................................................................243
12 ODC vs CDC OXYGEN DISSOCITION CURVE CARBONDIOXIDE DISSOCIATION CURVE PaO2 versus SpO2 PaCO2 versus CO2 in blood Sigmoid shaped: becoz of co-operativity Linear, steep, left ward Thus increasing ventilation preferentially increase O2 content in blood in low V/Q ratio areas of lung Thus increasing ventilation CO2 excretion increases both in high & low V/Q ratios. Less soluble CO2 is 20times more soluble Less diffusible More diffusible Perfusion limited: have equal alveolar & pulmonary capillary partial pressure, so the amount of gas content transferred is dependent on blood flow. (however diffusion limited in pathological condition:  high cardiac output:↓ pulmonary transit time  high altitude: ↓PaO2  alveolar-capillary barrier disease: ↓ surface area, ↑ thickness) (thus transit time in pulmonary capillary decreased during exercise by 2/3 to 0.25sec will not affect in normal individuals, however cause exercise induced hypoxemia in pathological conditions) Note: N2O is also perfusion limited. Ventilation limited However as its more diffusible, in impaired diffusion capacity: oxygen is affected more than CO2, leading to type I resp failure. Note: Carbon monoxide is diffusion limited Diffusion limited: gases which fail to equilibrate i.e the partial pressure of a substance in alveolous does not equal that in pulmonary capillary. Thus Even small Shunt will effect Thus Shunt up to 50% will not effect Oxygen transported in blood: 2forms: bound Hb, dissolved CO2: 3forms: dissolved (10%), carbonic acid(68%), bound Hb-carbamino(22%). 98% in RBC 75% in RBC, 25% in plasma Doesn‘t follow. Only dissolved part follow. Follows Henry‘s law: number of molecules in solution is proportional to partial pressure at liquid surface.  Bohr effect: the O2 delivery to tissue increases when pH↓(CO2↑) i.e affinity of O2 to Hb↓.  This effects is not significant for O2 delivery at tissues.  Haldane effect: Release of CO2 from blood to lung occurs when O2 conc increases. I.e CO2 affinity for Hb decreases as O2 increases.  This effect is significant for CO2 elimination (contribute 50%). Factors affecting: temp, pH, CO2, 2,3DPG, amount & type of Hb, CO, isoflurane, propranolol Right shift: sickle cell, thalassemia Left shift: fetal hb, carboxyhb, methemoglobin, sulfhemoglobin O2 shift curve to right 4 important points:  Arterial point: pO2 100mmHg with SaO2 98%  Saturation fall off point: pO2 60mmHg with spO2 90%: determine critical for fall in SpO2  Mixed venous point: pO2 40mmHg with SaO2 75%: determine oxygen consumption  P50: pO2 26.6mmHg with SaO2 50%: determine shift of curve 2 points: Arterial point: PCO2 40mmHg Mixed venous point: PCO2 46mmHg
Arrow represent Haldane effect
14 CXR PA vs AP view PA VIEW AP VIEW Scapula seen in periphery of thorax Scapula are over lung fields Clavicles are over lung fields Clavicles are above the apex of lung fields Posterior ribs are distinct Anterior ribs are distinct Heart is less magnified Heart is magnified Image is sharper Blurr Erect patient inspires more deeply showing more lung Ribs & clavicles are more horizontal Pleural air & fluid are more easy to detect on erect film
Respiratory failure types RESPIRATORY FAILURE TYPE I TYPE II TYPE III TYPE IV AHRF(acute hypoxic respiratory failure) Lung failure Ventilator failure Pump failure Periop respiratory failure Shock PaO2:↓↓(<60mmHg) ↓ ↓ ↓ PaCO2: normal or ↓ ↑↑(>50mmHg)(pH<7.35) normal ↑ PAO2-PaO2 gradient: >30 normal Bicarb: normal Normal/raised(always raised in acute on chronic type II resp failure) Mechanism: ↑ shunt Inadequate alveolar ventilation atelectasis ↓ perfusion of respiratory muscle Causes: V/Q mismatch Low ambient oxygen(high altitude, hypoxic gas) Pulmonary embolism ILD:  Pulmonary oedema  Pulmonary haemorrhage  Hypersecretory pneumonia  Sarcoidosis  IPF: idiopathic pulmonary fibrosis Shunts: >30%  ARDS  Atelectasis  Pneumonia  R→L shunt cardiac disease Hypoventilation:  Neuromucular diseases Diaphragmatic paralysis Myasthenia crisis GBS Brainstem lesion obesity  Chest wall abnormalities Kyphosvoliosis Severe ankylosis spondylitis obesity Airway disease:↑Dead space becoz Alveolar vent=(TV-dead space)x RR  Acute severe asthma  Severe COPD Post surgical atelectasis  Increased atelectasis due to low FRC  Anaesthesia  Obesity  Ascitis  posture Circulatory failure: Shock ↓ ↓perfusion of chest muscle ↓ Fatigue ↓ Chest muscle failure (hypoventilation) Treatment: Oxygen therapy PEEP/CPAP Supportive ventilation Respiratory stimulants O2, Sedative & narcotics are beneficial Sedative & narcotics are hazardous Caution when giving O2(as O2 can worsen hypercapnia) 𝑷𝑨𝑶𝟐 = 𝑭𝒊𝑶𝟐 𝑷𝑩 − 𝑷𝑯𝟐𝑶 − 𝑷𝒂𝑪𝑶𝟐 𝑹 𝑃𝑎𝐶𝑂2 = 𝐾 × 𝑉𝐶𝑂2 (1 − 𝑉𝑑 𝑉𝑡 ) × 𝑉𝐴 where PAO2 = alveolar partial pressure of oxygen, FiO2 = fraction of inspired oxygen, PB = barometric pressure (760 mm Hg at sea level), PH2O = water vapor pressure (47 mm Hg), PaCO2 = partial pressure of carbon dioxide in the blood, and R = respiratory quotient, assumed to be 0.8. where PaCO2 = the partial pressure of carbon dioxide in the blood, K = constant, VCO2 = carbon dioxide production, Vd/Vt = dead space ratio of each tidal volume breath, and VA = minute ventilation. Hypoxemic respiratory Analysis of the previous
16 failure with a widened alveolar–arterial oxygen gradient is caused by V/Q mismatching or shunt pathophysiology. These two processes can be differentiated by improvement of the hypoxemia with supplemental oxygen, in the case of V/Q mismatch, and no improvement in cases with shunt. equation shows that hypercapnia can occur from three processes:  an increase in CO2 production, which is extremely uncommon clinically as a sole cause for hypercarbia,  a decrease in minute ventilation by either a reduced tidal volume or respiratory rate, and  an increase in dead-space ventilation Note: that hypoxia refers to an oxygen deficit at a tissue level and depends on oxygen delivery. Therefore, cellular hypoxia can be a result of any process that affects oxygen delivery to the tissues, and includes:  Hypoxic hypoxia  Anemic hypoxia  Circulatory hypoxia  Histotoxic hypoxia Oxygen Delivery = Cardiac Output × Arterial Oxygen Content DO2 = CO × CaO2 DO2 = CO × (1.39 × [Hb (g/dL)] × SaO2) + (0.003 × PaO2) Note: Mixed respiratory failure(pathophysiologic process that can contribute to both hypoxia & hypercapnia) Seen in acute on chronic respiratory failure conditions, CO poisoning Cyanide poisoning(hypoxic hypoxia) CO poisoning(anemic hypoxia, pulmonary edema) Anticholinesterase poisoning Cyanide poisoning( respiratory arrest) CO poisoning( respiratory depressant, airway obstruction)
Hypoxemic respiratory failure Increased alveolar arterial gradient Normal alveolar arterial gradient Does PaO2 improve with supplement O2? Is PaCO2 elevated? Yes No V/Q mismatch Airway diseases  COPD, asthma, CF, BOS Interstitial lung disease  IPF, sarcoid, NSIP, DIP Alveolar filling  See list below Pulmonary vascular disease  Thromboembolism  Fat embolism Shunt Alveolar filling  Pulmonary edema  Left heart failure  Mitral valve disease  ALI/ARDS of any cause  Pneumonia  Trauma, contusion  Alveolar hemorrhage  Alveolar proteinosis  Drugs: heroin, paraquat  TRALI  Acute eosinophilic pneumonia  BOCP/COP  Aspiration  Upper airway obstruction  Near-drowning Atelectasis  Postoperative  Immobility Intrapulmonary vascular shunt  Pulmonary AVM  Hepatopulmonary syndrome Intracardiac shunt  PFO, ASD, VSD Yes No Hypoventilati- on (see below algorithm) High altitude low inspired PO2 ABBREVATIONS  CF: cystic fibrosis  BOS: bronchiolitis obliterans syndrome  IPF: interstitial pulmonary fibrosis  NSIP: nonspecific interstitial pneumonia  DIP: desquamative interstitial pneumonia  BOOP: bronchiolitis obiterans-organizing pneumonia  COP: cryptogenic organizing pneumonia  AVM: arteriovenous malformation
18 Hypercapnic respiratory failure Failure of one or more components of respiratory pump CNS Anterior horn cell Motor nerve Neuromuscular junction Muscle Airways & alveoli Excessive work of breathing  Drug effect (narcotics, sedatives)  Medullary stroke  Central apnea/hypoventilation syndrome  Metabolic alkalosis  Hypothyroidism  Idiopathic (Ondine‘s curse)  ALS/motor neuron disease  Poliomyelitis  Cervical spine injury  Guillian-Barre syndrome  Critical illness polyneuropathy  Fish toxin, tick paralysis, diphtheria toxin  Myasthenia gravis  Eaton-Lambert syndrome  Botulism  Organophosphate poisoning  Myopathy: drugs, steroids, infectious, critical illness, hypothyroidism  Muscular dystrophy  Polymyositis/dermatomyositis  Diaphragmatic dysfunction  COPD, asthma, cystic fibrosis  Pulmonary fibrosis  Pulmonary edema  Chest wall disorders, scoliosis  Obesity  Sepsis, metabolic acidosis  Upper airway obstruction  Tense ascitis, abdominal compartment syndrome
Pulmonary edema: cardiogenic vs non cardiogenic CARDIOGENIC NON - CARDIOGENIC Types Flash Pulmonary Edema 1. ARDS 2. Re-expansion PE 3. High altitude PE 4. Reperfusion PE 5. Neurogenic PE 6. Drug induced PE Definition fluid transition from pulm cappilaries to interstitium and alveoli due to elevated pulm venous and left atrial pressures; without change in the permeability or integrity of the endothelial and epithelial layers of the pulmonary capillaries It is a manifestation of increased permeability of the pulmonary capillaries in which cardiac function is relatively preserved. Pulmonary artery wedge pressure ≤18 mmHg. Predisposing factor 1. LV systolic dysfunction 2. Diastolic dysfunction 3. Coronary heart disease 4. Hypertension 5. Valvular heart disease 6. Idiopathic dilated cardiomyopathy. 7. Toxins (e.g., anthracyclines) 8. Metabolic disorders (e.g., hypothyroidism) 9. Viral myocarditis (e.g., Coxsackie B virus or echovirus infection). 10. Chronic disorders : left ventricular hypertrophy of any etiology, hypertrophic and restrictive cardiomyopathies. 11. Acute causes : ischemia, acute hypertensive crisis 12. Left atreial or ventricular outflow obstruction - History & physical examiniation  H/o MI, CHF, valvular heart disease  S3 gallop, murmurs  Cold extrimities  Hypoxia – V/P mismatch – usually corrected by oxygen  H/o infections, aspiration, trauma, major surgeries, drug intake  Hypoxia – intrapulmonary shunt – not improved by oxygenation CXR  Cardiomegaly  Kerley B lines and loss of distinct vascular margins  Cephalization: engorgement of vasculature to the apices  Perihilar alveolar infiltrate  Pleural effusion  Vascular pedicle width >70mm  Heart size is normal  Uniform alveolar infiltrate  pleural effusion is uncommon  lack of cephalization  Vascular pedicle width <70mm Echocardiogram  Enlarged chamber  LV dysfunction present  Normal chamber size  No LV dysfunction Pulmonary Artery Catheterisation PAOP > 18 mmHg PAOP < 18 mmHg
20 Response to treatment Generally have an identifiable cause of acute LV failure—such as arrhythmia, ischemia/infarction, or myocardial decompensation that may be rapidly treated, with improvement in gas exchange. Usually resolves much less quickly, & most patients require mechanical ventilation. Treatment general principle:  Emergency management o Upright Sitting Posture o Support of oxygenation and ventilation  Oxygen therapy/positive pressure ventilation  Reduction of pre load & Inotrope support o Loop diuretics, Nitrates(NTG), Morphine  Conditions that complicate PE must be corrected o Infection, myocardial ischaemia, Renal failure, Anemia Reexpansion pulmonary edema  Diuretics and preload reduction are contraindicated, and intravascular volume repletion often is needed while supporting oxygenation and gas exchange. High altitude pulmonary edema  It can be prevented by use of dexamethasone, calcium channel– blocking drugs, or long-acting inhaled β2-adrenergic agonists.  Treatment includes descent from altitude, bed rest, oxygen, and, if feasible, inhaled nitric oxide; nifedipine may also be effective. HBOT.
ARDS vs CHF vs Pneumonia Distinguishing factor ARDS CHF PNEUMONIA Symptoms Dyspnea + + + Hypoxia + + + Pleuritic chest pain +/- - + Sputum production +/- - + Tachypnea + + + Signs Edema - + - Fever +/- - + JVP raise - + - Rales + + + Third heart sound - + - Investigations B/L infiltrates + +/- +/- Cardiac enlargement - + - Elevated BNP +/- + - Hypoxemia + + + Localized infiltrate - - + PAO2/FiO2 ratioo <300 + - - PCWP <18mmHg + - + Response to Rx Antibiotics - - + Diuretics - + - Oxygen - + +
22 ARDS H vs L ARDS-Corona associated{CARDS}-Gattinoni’s dichotomanoius model H TYPE L TYPE High elastance(low compliance)-stiff lungs Low elastance(normal compliance) High lung weight Low lung weight High response to PEEP Low response to PEEP High recuritability Low recruitability High Right to left shunt Low ventilation perfusion ratio Baby lung( progression of L-type to H-type) Hypoxia due to Lungs lost HPV response, imbalance b/w angiotensin II & Angiotensin 1-7, pulmonary vascular thrombosis Rest of causes for ARDS & COVID-19(20-30%) Associated with COVID-19(70-80%) Most common form of ARDS(typical form) rare Require low TV & High PEEP for management Require high/normal TV and low PEEP PEEP beneficial PEEP harmful ?Antiinflammatory beneficial ?Anticoagulants beneficial
Obstructive vs restrictive lung OBSTRUCTIVE RESTRICTIVE Airways Obstructed at any level from trachea to respiratory bronchiole Reduced expansion of lung parenchyma CXR Variable appearance depending upon the cause Typically bilateral infiltrates giving ground-glass shadows Examples • Chronic bronchitis • Emphysema • Bronchial asthma • Bronchiectasis • Chest cage disorders (e.g. kyphoscoliosis, poliomyelitis, severe obesity and pleural disease) • Interstitial lung diseases (ILDs) (e.g.pneumoconioses, idiopathic pulmonary fibrosis, immunologic lung diseases, collagen-vascular disease and sarcoidosis) PFT FEV1 ↓ ↓ FVC N ↓ FEV1/FVC ↓ N FRC ↑ ↓ TLC ↑ ↓ Raw ↑ N FEV25-75% ↓ N MBC ↓ N PEFR ↓ ↓
24 Chronic bronchitis vs Emphysema CHRONIC BRONCHITIS EMPHYSEMA Diagnosis Clinical: >3m cough for subsequent 2y Pathological: abnormal dilation of respiratory bronchioles & alveoli due to airflow obstruction Age 40-45y 50-75y Dyspnea Mid, late Severe, early Cough Early, before dyspnea Late, after dyspnea Sputum Copious, purulent Scanty, Appearance Blue bloater Pink puffer Infections common occasional Pathogenesis Impaired ciliary activity Deficiency of α1-antitrypsin Respiratory insufficiency repeated terminal PaCO2 50-60mmHg 35-40 PaO2 45-60 65-75 DLCO Normal to slight reduction Decreased Corpulmonale common Rare, terminal Airway resistance increased Normal or slightly increased Elastic recoil normal low CXR Prominent vessels, large heart Hyperinflation, small heart
CHRONIC BRONCHITIS vs SMALL AIRWAYS DISEASE vs ASTHMA vs BRONCHIECTASIS CHRONIC BRONCHITIS SMALL AIRWAYS DISEASE ASTHMA BRONCHIECTASIS Location Bronchus(1-16th gen) Note: Brochus1-3 Bronchioles 4-19 Small airway 17-23 Bronchiole (17- 23rd gen) Bronchus Bronchus Age at diagnosis Adults Children Extrinsic: children Intrinsic: adults Adults Etiology Smoking, air pollution Viral infection, connective tissue disorder smoke Extrinsic: allergy Intrinsic: viral infection Infection, obstruction Pathogenesis Impaired ciliary Movement Damage to surfactant IgE-sensitised mast cells Damaged airways Major gross feature Thickened bronchial wall Occluded bronchioles Overdistended lungs Dilated bronchi and bronchioles Main histology Hyperplasia of mucous glands Fibrous plugs in bronchioles Mucus plugs in bronchioles Inflammed bronchi Major clinical feature Persistent cough with expectoration Cough, dyspnoea Bronchosplasm Copious foul-smelling expectoration
26 Lobar Pneumonia Vs Bronchopneumonia Vs Interstitial Pneumonia LOBAR PNEUMONIA BRONCHOPNEUMONIA INTERSTITIAL PNEUMONIA Definition Acute bacterial infection of a part of a lobe of one or both lungs, or the entire lobe/s Acute bacterial infection of the terminal bronchioles extending into adjoining alveoli. Also called lobular pneumonia Interstitium . Also called Hamman- Rich syndrome, Atypical pneumonia Age group More common in adults Commoner at extremes of age– infants and old age Commoner at extremes of age–infants and old age Predisposing factors More often affects healthy individuals Pre-existing diseases e.g. chronic debility, terminal illness, flu, measles immunocompramised Common etiologic agents Pneumococci, Klebsiella pneumoniae, Staphylococci, Streptococci Staphylococci, Streptococci, Pseudomonas, Haemophilus influenzae Viruses PJP Mycoplasma Chlamydia Pathologic features Typical case passes through stages of congestion (1-2 days) , early (2-4 days) and late consolidation (4-8 days), followed by resolution (1- 3 weeks) Patchy consolidation with central granularity, alveolar exudation, thickened septa Diffuse alveolar damage, interstitial edema composed of lymphocytes, type 2 pneumocyte Clinical features Consolidation features which is Unilateral, limited by anatomical boundaries Consolidation features with Bilateral, asymmetrical, not limited by anatomical boundaries Diffuse rales Investigations Neutrophilic leucocytosis, positive blood culture Neutrophilic leucocytosis, positive blood culture Lymphopenia, eosinophilia, HRCT CXR consolidation mottled focal opacities Diffuse hazy opacities, septal thickening USG consolidation Patchy B-lines, may show consolidation Patchy B-lines, may show consolidation Prognosis Better response to treatment, resolution common, prognosis good Response to treatment variable, organisation may occur, prognosis poor poor Complications Less common; pleural effusion, empyema, lung abscess, organisation Bronchiectasis may occur; other complications same as for lobar pneumonia fibrosis
DLT, Bronchial blockers: Advantage vs Disadvantages ADVANTAGES DISADVANTAGES DLT Easy to place successfully Size selection more difficult Repositioning rarely required Difficult to place in patients with difficult airways or abnormal tracheas Bronchoscopy, Suction & CPAP to isolated lung is easily added Potential laryngeal trauma Can alternate OLV to either lung easily Potential bronchial trauma Placement still possible if bronchoscopy not available Not optimal for postoperative ventilation Best device for lung isolation BRONCHIAL BLOCKERS Easily added to regular ETT Positioning-more difficulty Difficult/abnormal airways Blind insertion less successful Children Right lung collapse difficult due to RUL anatomy Trachesotomised patient Displacement/repositioning more common, needs FOB Limited access to isolated lung-CPAP Limited access to isolated lung-min suction, bronchoscopy Accurate size not required Alternating isolation of lungs more difficult Allows ventilation during placement Selective lobar isolation possible Change of tube not required for postoperative ventilation
28 Bronchial blockers Cohen Blocker Arndt Blocker Fuji Uniblocker EZ-Blocker Size 9-Fr 5-Fr, 7-Fr, and 9-Fr 5-Fr, 9-Fr 7-Fr Balloon shape Spherical Spherical or elliptical Spherical Spherical × 2 Guidance mechanism Wheel device to deflect the tip Nylon wire loop that is coupled with the fiberoptic bronchoscope None, preshaped tip None Smallest recommended ETT for coaxial use 9-Fr (8.0 ETT) 5-Fr (4.5 ETT), 7-Fr (7.0 ETT), 9-Fr (8.0 ETT) 9-Fr (8.0 ETT) 7.5 ID Murphy eye Present Present in 9-Fr Not present No Center channel 1.6 mm ID 1.4 mm ID 2.0 mm ID 1.4 mm ID bronchial blocker has a high-volume, low- pressure cuff. bronchial blocker has a high-volume, low-pressure cuff. Y-shaped with the bifurcation of the main-stem into two distal extensions to be placed in both main-stem bronchus inner lumen contains a flexible nylon wire which exits as a small flexible wireloop. The wire loop is coupled with the fiberoptic bronchoscope and serves as a guide wire central lumens of both stems extend into the main shaft and with ports to suck out secretions or CPAP Once inserted repositioning very difficult as wire guidance not possible
Cohen Arndt Fuzi Ez
30 NTG vs SNP NTG SNP Chemistry Organic Inorganic: five CN and one NO combined Preparation Oral, SL, Patch & Injectable Injectable Injectable available as Solution Powder form-to be reconstituted. Protect from light & use in 12hrs. Stability Absorbed by some plastic(upto80%) Stored in glass vials Unstable in light & alkali. Stored out of light: alumini foil MOA NTG+Endothelium→N2O→NO Via gluthione S-transferase SNP+Hb→Methemoglobin+CN+NO NO act on SH group of smooth muscle → stimulate cGMP by ↑ Guanyl cyclase enzyme→smooth muscle relaxation. NO released by enzymatic nteraction NO released spontaneously(non enzymatic activation) Systemic action  At low doses Venous>arterial (selective): so preload reduction  Thus disrupts renal autoregulation  Bronchodilation, Pul, Vasodilation→↑shunt  ↑ICP  Antiplatlet action  Used in angina  Act equally on veins & arteries (non selective) so no regional effect. Both preload & after load reduction.  Thus renal blood flow maintained  Attenuates HPV→↑Shunt  ↑ICP becoz of ↑CBF: only in early stage Pharmaacokinetics: Absorption  Very high first pass metabolism(upto 95%)  Rapid aabsorption via other routes  Only IV preparation Distribution Large-60% protein bound Not known Metabolism Hepatic→Thiols Rapid liver rhodanase→ prussic acid→ thiocyanate (eliminated in 3-7days) Elimination 2-4min via urine 2-4min via urine Side effects Hypotension with tachycardia Tolerance Methemaglobin(so ↓O2 carrying capacity) Hypotension with tachycardia No tolerance Becoz of thiocyanite Nausea, vomiting, pain abdomen, hypereflexia, seizure Rebound HTN Long term: cyanide toxicity methemoglobin Coronary steal Coronary blood flow MI - ↑ ↓ + ↓ ↑ Cardiac output ↓↑ ↑ MAP ↓ ↓↓ SVR ↑ ↓ Pul VR ↓ ↓↓
Head ache + - Dose 5-50mcg/min Toxicity:  For siginificant methemoglobinemia: 250mcg/min for 7days 0.2-10mcg/kg/min Toxicity:  For cyanide toxicity:  Not more than 0.5mg/kg/hr or 2mcg/kg/min. Plasma CN conc to be < 3µmol/l.  For thiocyanate toxicity: 2- 5mcg/kg/min for 7-14days.  For 10% methemoglobin formation 10mg/kg.
32 Cardiac tamponade vs constrictive pericarditis CARDIAC TAMPONADE CONSTRICTIVE PERICARDITIS After systole here slow expansion ↓ So gradual descent of y After systole its fast ↓ So pericardial knock & rapid y descent - Rapid y descent[PAY TAX] Rapid x descent [PAY TAX] +/- Kussmaul sign: absent [becoz pericardium can still expand] Present [normally JVP fall during inspiration as negative pressure in mediastinum. In constrictive pericarditis no effect of inspiration leading to negative pressure change in pericardium, so JVP rise during inspiration] Pulsus paradox: +++. Inspiration → RV dilation → pressure in pericardial fluid ↑ → LV pushed in → ↓ LV filling→↓SBP. + Inspiration→ RV dilation → septum move to LV →↓LV filling→↓SBP. Equalisation of diastolic pressure:+ + Becks triad[hypotension, rised JVP, muffled heart sounds], Moschcowitz triad[widening of cardiac flatness, abrupt transition from pulmonary to cardiac flatness, wiening of cardiac dullness in second intercostals space], ECG triad[S tachy, Low voltage, electrical alternans), POCUS triad[pericardial fluid, RV diastolic collapse, dilated IVC] Triad of pericardial knock, raised JVP, retractile apex in the setting TB - Pericardial knock Low voltage ECG: ++ Electrical alternans:++ ++ - Apex not identifiable Retractile apex - Square root/dip & plateau sign in diastolic waveform Acute/chronic chronic Treatment: pericardiocentasis Pericardial stripping
Constrictive pericarditis vs restrictive cardiomyopathy CONSTRICTIVE PERICARDITIS RESTRICTIVE CARDIOMYOPATHY HFpEF HFpEF Pericardial Diastolic heart failure Myocardial Diastolic heart failure JVP: raised raised Square root/dip & plateau sign in diastolic waveform: frequent Square root/dip & plateau sign in diastolic waveform: rare Equalisation of pressure: frequent Rare(usually L>R) Kussmaul sign: present present chronic chronic Predominant right sided heart failure Right &/ or left Prominent y descent Variable y descent Pulsus paradox: usually absent rare - Conduction abnormality : common Idiopathic, following Sx, RT Primary or infiltrative, drug, RT History of pericarditis(peluritic chest pain, fever, cardiac surgery, trauma, RT, connective tissue disorder): + - Dissociation of intrathoraxic & intracardiac pressure: discordant Rt & Lt ventricle peak systolic pressures Are in phase Enhanced ventricular interdependence: movement towards left ventricle on inspiration little Pericardial knock Third heart sound MR, TR: absent Present often On Echo: E‘: normal or increased Decreased( ventricular speckling in amyloidosis) MRI/CT: pericardial thickening - Endomyocardial biopsy: not useful useful Treated with pericardiectomy, anti-inflammatory Conservative, stem cell transplant, cardiac transplant Prognosis: good poor ANESTHESIS MANAGEMENT: also same for cardiac tamponade  Positive pressure ventilation is dangerous( decrease venous return)  Avoid decrease in HR, cardiac contractility, SVR(thus ketamine is useful) AF is dangerous
34 Inotropes: Dopamine vs Dobutamine vs Adrenaline vs Noradrenaline DOPAMINE DOBUTAMINE ADRENALINE NORADRENALINE Preparation Clear, colorless solution for injection containing 40mg/ml of dopamine hydrochloride  Vials containing 250mg of dobutamine hydrochloride and 250mg mannitol in a lyophilised form.  It is also available as 20 ml vial containing 250mg of dobutamine hydrochloride (12.5mg/ml) with 4-8 mg of sodium bisulphite dissolved in water.  50mg/ml 5ml ampoule  Clear solution for injection containing 1mg/ml of adrenaline hydrochloride.  Also comes as aerosol spray delivering 280 μg metered dose of adrenaline acid tartrate. As a clear colourless solution for injection containing 2 mg/ml of noradrenaline acid tartrate Chemical origin Catecholamine synthetic isoprenaline derivative catecholamine catecholamine t1/2 1min 2.4min 2min 3min Dose  Renal dose 0.5-2 μg/kg/min  β1 action 2-10 μg/kg/min  α & β1 action 10-20 μg/kg/min  endogenous noradrenaline release at dose >5 μg/kg/min 2.5 - 10 μg/kg/min ; occasionally upto 40 μg/kg/min Pressor support  1–2 μg/min predominantly activates β2 receptors leading to vascular and bronchial smooth muscle relaxation  2 – 10 μg/min β1 and β2 action. Heart rate,contractility and conduction through AV node increased.  >10 μg/min marked α stimulation and generalized vasoconstrictions CPR  1 mg (ie 0.02 mg/kg) IV stat is given for asystole, VF  In situations where IV access is not available adrenaline 0.01- 0.5 μg/kg/min.
dose is tripled and diluted in 10 ml saline, to be given via endotracheal tube or intraosseous route. Bronchodilation:-  Due to its vasoconstrictive action adrenaline is used to reduce airway obstruction caused by oedematous mucosa in patients of severe croup, post extubation & traumatic airway edema.  Adrenaline is used for nebulization in such patients. Effect of each nebulisation lasts for around half to one hour. 0.05ml/kg(max 1.5cc) diluted to 5cc with NS.  Subcutaneous injection of adrenaline is also used for this purpose. Dose is 300μg (1/3rd ampoule) every 20 minutes. Upto 3 such doses can be given. Mechanism of action Has 2 mechanisms of action one is via direct stimulation of receptors and second is via indirect release of noradrenaline Direct Action:-  Low doses:- It stimulates dopaminergic receptors D1 and D2  D1 causes mesenteric and renal bed Predominantly β adrenergic receptor stimulating agent (β1 > β2>α)  At lower doses it causes β stimulation.  At higher doses α stimulation predominates.  The drug causes β mediated rennin release. This indirectly potentiates the vasoconstrictor action.  This drug exerts its action predominantly at α – adrenergic receptors, with a minor action on beta receptors.  Noradrenaline when given exogenously (ie. Via intravenous route) can produce bradycardia while endogenous release of the drug evokes
36 vasodilatation  β action begins at around 3μg/kg/min  Beyond 10 μg/kg/min α action predominates Indirect Action:- Its indirect action is via release of noradrenaline. This action begins at a dose of 5μg/kg/min. Prolonged use of dopamine causes depletion of noradrenaline stores and decreased response to the drug. tachycardia. HEART  Produces positive inotropic effect by stimulating β1 receptors.  Heart rate is increased due to positive chronotropy  Force of cardiac contraction (positive inotropism) is increased via direct β1 action.  Afterload is decreased due to β2 mediated fall in peripheral vascular resistance.  Increase in cardiac contractility along with fall in afterload causes improvement in CHF patients.  Left ventricular end diastolic volume reduces and organ perfusion improves.  It has both positive inotropic and positive chronotropic effect on heart.  As a result myocardial oxygen demand is also increased.  It is the drug of choice at the end of cardiopulmonary bypass when maximal inotropic effect is required.  Conduction through AV node improves and AV block if present is reduced.  It causes increase in peripheral vascular resistance leading to rise in blood pressure.  Cardiac output remains unchanged or decreases slightly as heart has to work against increased afterload.  This also results into increased myocardial oxygen demand. QT prolongation: + + + + Blood vessels  E ndogenous norepinephrine release produced by dopamine causes considerable vasoconstriction.  Moreover this  Vasodilation occurs due to β2 action on blood vessels.  At lower doses β mediated vasodilation.  While at higher doses vasoconstriction predominates leading to increase  It causes α mediated increase in peripheral vascular resistance leading to increase in blood pressure.
drug has no major action on β2 receptors and therefore unopposed stimulation of α1 receptors is responsible for overall vasoconstriction.  At low doses D1 mediated splanchnic & renal vasodilation occurs. in SVR RS  Ventilatory response to hypercapnia and hypoxia is reduced by dopamine due to action on dopaminergic receptor located in the carotid bodies (Peripheral chemo receptors).  Increases pulmonary artery pressure -  It is a respiratory stimulant though this action is not very significant clinically.  It is a potent bronchodilator due to βaction.  It reduces vocal cord edema in patients of croup α1 mediated vasoconstriction. It causes slight increase in minute volume along with some degree of bronchodilatation CNS  Probably causes vasodilation of normal cerebral vasculature with no effect on CMR.  Very high dose may cause cerebral vasoconstriction.  Exogenous dopamine does not cross BBB except in its levo-rotatory form.  It also stimulates CTZ leading to nausea.  Increases CMR and cerebral blood flow at high doses.  No or minimal effect is seen in low doses.  BBB defect exaggerates the phenomenon.  It penetrates CNS to a limited extent.  CMR & CBF are increased especially when BBB is open.  It does not have much effect on CBF & CMR when BBB is intact.  Cerebral vasodilation & increase in CMR occurs when BBB is open. Kidney  At low doses causes marked  Increase in cardiac output  RBF is reduced by 40%, although GFR ↓RBF
38 renal vasodilatation leading to corresponding ↑RBF  Increase in urine output is also due to interference with renal tubular function.  At higher doses vasoconstriction predominates and the advantage on RBF is lost. causes increase in urine output.  Specific action on RBF is absent. may remain minimally altered.  Increase in sphincter tone and decrease in bladder tone may cause difficulty in micturition. GIT Splanchnic blood flow is increased due to action on DA1 receptors.  Total increase in cardiac output improves organ perfusion.  Direct action on gastrointestinal vasculature is not present.  Intestinal tone & secretions are decreased.  Splanchnic blood flow is increased when used in β dose  Vasoconstriction predominates at higher doses. Hepatic & splanchnic blood flows are decreased. Pregnant uterus Inhibits contractions of pregnant uterus. Increases contractility of the pregnant uterus, may cause fetal bradycardia & asphyxia. Metabolic & other effects Release of prolactin, growth hormone & aldosterone are depressed. -  ↓ insulin secretion.  Glucagon secretion is ↑ resulting into rapid glycogenolysis & raised blood sugar levels.  ↑ in activity of lipases causes increased concentration of FFA (free fatty acids) in blood.  BMR ↑ by 20 – 30%  Renin activity is ↑ in plasma.  Decreases insulin secretion leading to hyperglycemia.  Plasma rennin activity rises.  FFA concentration is ↑
Pharmacoki netics  One fourth of the administered dose is converted to noradrenaline within adrenergic nerve endings.  Metabolites are excreted in urine either as such or after glucuronide conjugation. Also excreted in feces Natural endogenous catecholamine Synthetic derivative Natural endogenous catecholamine Natural endogenous catecholamine Nonchiral compound Two isomers present: L(–) and R(+) Two isomer Vd 1.8–2.5 l/kg 0.2 l/kg Side-effects Raise blood sugar Raised IOP Nausea & vomiting Potentiates development of MODS Reduce blood sugar Allergy present Contraindic ations Pulmonary HTN, cor pulmonale Aortic stenosis, mitral stenosis Shock  Cardiogenic without arrhythmia  Cardiogenic SBP 70-90  Cardiogenic with SBP>90  Pulmonary embolism, cor pulmonale  CPR  Cardiogenic(2nd line)  Septic(2nd choice)  Anahylactic  neorogenic  Cardiogenic with arrhytmia  Cardiogenic SBP<70  septic α 1 ++ + +++ +++ α 2 + - ++ +++ β 1 ++ +++ +++ + β 2 +++ + ++ - D +++ - - - Inotrope+vasopresso r inodilator Inotrope+vasopressor Inotrope+vasopressor HR + + ++ - MAP ++ + + +++ Dopamine ↓ ↓ Homovanilic acid ↓ 3,4 dihydroxy phenyl acetic acid MAO & COMT Dobutamine ↓ ↓ 3-Omethyl dobutamine (inactive) ↓ Glucuronide conjugation ↓ Excreted in urine mainly COMT Adrenaline ↓ ↓ Metadrenaline & normetadrenaline ↓ 3 methoxy 4 hydroxyphenyl ethylene + 3 methoxy 4 hydroxy mandelic acid ↓ Excreted predominantly in urine COMT Noradrenaline ↓ ↓ Methylation & oxidative deamination of compound ↓ VMA Predominant metabolie; Excreted in urine (3 methoxy, 4 hydroxy mandelic acid) MAO & COMT
40 SVR + - +/- +++ Inotropy ++ ++ ++ + CO +++ +++ ++ +/- Arrhythmia ++ + ++ + Increased myocardial O2 demand + - + + Main harmone of adrenal medulla Main neurotransmitter of sympathetic system
Meph vs Phenylephrine vs Ephidrine VASOPRESSORS SYNTHETIC NONCATECHOLAMINES SYMPATHOMIMETICS PHENYLEPHRINE EPHEDRINE MEPHENTERAMINE MOA Selective α1 receptor agonist at clinical doses, increasing systemic vascular resistance secondary to vasoconstriction. Primarily causes venoconstriction.  α and β receptor agonist.  Both direct and indirectly acting , clinical effect is primarily due to its indirect action of releasing norepinephrine from postganglionic nerve endings  α and β receptor agonist.  Both direct and indirectly acting ADVANTAGES  Immediate onset  short duration of action 10-15 minutes  Ideal for continuous infusion  Economical  Does not need multiple dilutions as compared to Phenylephrine.  No bradycardia  Economical  Does not need multiple dilutions as compared to Phenylephrine ,  immediate onset of action peaking at 5 min and lasting 15-30 min DISADVANTAGES  Tachyphylaxis.  Reflex bradycardia and  serial dilution for IV administration is source of error  genetic polymorphism lead to variable response  Tachyphylaxis.  Tachycardia,  Adverse effect on fetal acid base status  as compared to Phenylephrine delayed onset of action,  longer duration of action of about 60 min  attenuated response with cocaine, reserpine  accentuated response in patient on MOA inhibitors  Tachyphylaxis.  Little evidence available on placental transfer and its foetal metabolic impact IV Preparation 10mg/ml 50mg/ml 30mg/ml Other actions  Particularly useful in patients with coronary artery disease and in patients with aortic stenosis because it increases coronary perfusion pressure without chronotropic side effects, unlike most other.  Nasal spray is a 1% solution for decongestion  chronic oral medication to treat bronchial asthma  acute coryza  0.5 mg/kg intramuscularly, has an antiemetic effect  Nasal decongestant  Stimulant in psychiatry
42 CNS stimulation is minimal Causes hyperkalemia (opposite of beta action) Mydriasis accompanies the administration of ephedrine, and CNS stimulation does occur CNS stimulant Duration of action 15min 60min 30min F/M Ratio 0.17 0.71 Metabolism MAO deaminated by MAO in the liver, and hepatic conjugation also occurs. The slow inactivation and excretion of ephedrine are responsible for the prolonged duration of action n-demethyation in liver microsome Elimination <0.5% excreted unchanged in urine 40% excreted unchanged in urine urine Bolus dose 50-200mcgIV 5-10mg IV 3-6mg IV Infusion 20-100mcg/min - -
Racemic adrenaline vs L adrenaline RACEMIC ADRENALINE L-ADRENALINE Strength: 2.25% i.e 22.5mg/ml 0.1% [1:1000] i.e 1mg/ml Contain both L & D form @ 1: 1 ratio L-form is most active Not available in India(available only in USA) Readily available Was preferred for nebulisation over more active & more readily available l-epinephrine to minimize anticipated CVS side effects such as tachycardia & HTN Can be used. Found to be equally effective & does not carry risk of additional adverse effect Dose for nebulisation: 0.05ml/kg(max of 0.5ml i.e 11.25mg) of 2.25% solution with 2.5ml NS 0.5ml/kg (max of 5ml i.e 5mg) of 1:1000 solution with 4-5ml NS Costly Less expensive
44 Calcium gluconate vs calcium chloride CALCIUM CHLORIDE CACIUM GLUCONATE Elemental calcium content: 13.6mEq/gm of Calcium (3times more potent) 4.65mEq/gm 1gm/10ml: 10% 1gm/10ml: 10% Osmolarity: 2000mOsm/l 680mOsm/l Available calcium: 27.2% 9.3% Preferred administration via central line Peripheral administration Can cause tissue necrosis Risk of tissue necrosis & phlebitis is less Dilute (20mg/ml) & administer at slower rate 1gm over 10min Can be given slow IV push Preferred in cardiac arrest & poor liver function. However 1/3rd of dose is used. Require hepatic metabolism for removal of gluconate and formation of active Ca 2+ . So in setting of poor liver function & cardiac arrest (emergency) it is not preferred.
Type I vs Type II MI TYPE I TYPE II Acute atherothrombotic coronary event Acute imbalance between oxygen supply (eg. Hypoxemia, anemia, hypotension, vasospasm ) and demand (eg. Tachycardia, anemia, hypertension, surgical stress). No coronary artery disease. Chest pain more common symptom Dyspnea Initial presentation suggestive of MI Non cardiac problem (sepsis, trauma, hemorrhage) Amount of clinical stress low High (high dose vasopressors, anemia, hypoxemia, hypotension) STEMI or NSTEMI ST depression Echo : new RWMA, reduced EF Hyperkinetic, underfilled heart Troponin elevation: more Moderate Evidence based treatment established no Reperfusion strategy (invasive), anticoagulants Frequently managed non-invasively & received less frequently cardio-protective drugs Treat underlying cause Note: Type 3: sudden unexpected cardiac death often with symptoms suggestive of myocardial ischemia Type 4: associated with percutaneous coronary intervention or stent thrombosis Type 5 : associated with cardiac surgery MINS: myocardial injury after noncardiac surgery. Troponin elevation apparently from cardiac ischemia with or without signs, symptoms and ECG changes.
46 Myocardial stunning vs myocardial hibernation vs infraction MYOCARDIUM STUNNING HIBERNATION INFRACTION Regional dysfunction + + + Tissue perfusion Uncoupling (flow normal, muscle function ↓) Coupling (flow ↓, muscle function ↓) Coupling (flow -, muscle function-) pathogenesis Relief of ischemia: transient post ischemic dysfunction Persistent ischemia(survival hypothesis), repetitive stunning hypothesis, smart heart hypothesis Necrosis, scarring Onset Sudden following ischemia and reperfusion event: stress/CABG/stent After weeks or months of ischemia Acute: thrombotic Chronic: stenotic Resolution 6-8hrs post CPB Delayed, days to months following revascularisation absent Inotropic support Has effect on stunned myocardium Has effect No effect Revascularisation Beneficial beneficial Not beneficial PET scan/ MRI Viable viable Non viable
Alpha stat vs pH stat ALPHA STAT METHOD pH STAT METHOD It considers the alkaline pH seen during CPB is physiological (increased solubility of carbon dioxide seen during hypothermia raises the pH.) pH & Pco2 are maintained at normal values regardless of the body temperature. no additional measures to correct the pH/ PCO2 levels are undertaken. In order to maintain PCO2, CO2 is added to the ventilating gas mixture. more commonly used method This method is not preferred preserve cerebral autoregulation & improve myocardial preservation. patients tend to have higher CBF because of increase in CO2 content and there will be loss of cerebral auto regulation. More flow, more chances of micro- embolization. Blood pH : alkalotic Normal Intracellular pH : normal acidotic Intracellular enzyme function: maintained decreased Technically demanding: no Yes[require adding of CO2] Total CO2 content kept constant [pH & pCO2 vary with temp] pH kept constant Advantage 1. Better enzyme function 2. ↓CBF coupled with ↓energy 3. Coupling independent of cerebral perfusion pressure 4. Less arryhythmia 5. Better cerebral recovery 6. ↓microemboli Advantage 1. ↑CBF global cerebral cooling (↓O2 consumption) 2. Better flow to deep brain structure Better in adults [less stroke] Better in children [good oxygenation] Disadvantage • ↓CBF Disadvantage • Brain injury↑: because 1. ↑micremboli 2. ↑ICP 3. Cerebral edema 4. Steal phenomena 5. Abolition of cerebral autoregulation 6. Redistribution away from marginally per fused area
48  PaO2 ↓ by 5mmHg for each degree below 37 0 C  PaCO2 ↓ by 2mmHg for each degree below 37 0 C  Change in pH=0.015pH units/degree change in temp  However electrical neutrality has to be maintained, so protein like histidine imidazole play role in maintaining it. Alpha = unprotinated histidine imidazole / [H+ ] Variable +1 o C -1 o C pH -0.015 +0.015 pCO2 +0.27kPa (2mmHg) -0.27kPa (2mmHg) pO2 +0.6kPa (5mmHg) -0.6kPa (5mmHg) Combination of alpha & pH stat: Goal: maintain constant pH during cooling & restore electrochemical neutrality before circulatory arrest. Method: Use temperature corrected values during cooling & rewarming. Temperature uncorrected values in between. CO2 initially increases during cooling. Advantage: produce homogenous brain cooling, then restore neutrality, improves CMRO2. During CPB Hypothermia for organ protection @20 0 C CO2 solubility ↑ ↓PaCO2 [as temp↓→solubility ↑→pressure↓] @ 37 0 C CO2 solubility ↓ ↑PaCO2 @20 0 C H2O→H+ + OH- Reaction is inhibited So H+ ↓and pH ↑ @ 37 0 C H2O→H+ + OH- Promoted So H+↑ and pH↓
Aortic clamping vs unclamping AORTIC CROSS CLAMPING AORTIC UNCLAMPING HEMODYNAMIC CHANGES  ↑ Arterial BP above the clamp  ↓ Arterial BP below the clamp  ↑ Segmental wall motion abnormalities  ↑ Left ventricular wall tension  ↓ Ejection fraction  ↓ Cardiac output  ↓ Renal blood flow  ↑ Pulmonary occlusion pressure  ↑ CVP  ↑ Coronary blood flow HEMODYNAMIC CHANGES  ↓ Myocardial contractility  ↓ Arterial blood pressure  ↑ Pulmonary artery pressure  ↓ CVP  ↓ Venous return  ↓ Cardiac output METABOLIC CHANGES  ↓ Total-body oxygen consumption  ↓ Total-body carbon dioxide production  ↑ Mixed venous oxygen saturation  ↓ Total-body oxygen extraction  ↑ Epinephrine and norepinephrine  Respiratory alkalosis  Metabolic acidosis METABOLIC CHANGES  ↑ Total-body oxygen consumption  ↑ Lactate  ↓ Mixed venous oxygen saturation  ↑ Prostaglandins  ↑ Activated complement  ↑ Myocardial depressant factor(s)  ↓ Temperature  Metabolic acidosis FACTORS INFLUENCING  Level of aortic cross-clamp  Species differences  Anesthetic agents and techniques  Use of vasodilator therapy  Use of diverting circulatory support  Degree of periaortic collateralization  Left ventricular function  Status of the coronary circulation  Volume status  Neuroendocrine activation  Duration of aortic cross-clamping  Body temperature  Duration & location of the aortic clamp determine the degree of hypotension observed  A supraceliac clamp can result in significant bowel & liver ischemia; decrease in SVR & CO after release of such a clamp can be significant THERAPEUTIC INTERVENTIONS  Anticipation of the increase in SVR is important  Heparinisation before clamp  Some vascular surgeons clamp the iliac arteries first to prevent distal embolization due to the aortic clamp AFTERLOAD REDUCTION  SNP  Inhaled anesthetics  Amrinone –PDE3#  Shunts and aorta-to-femoral bypass PRELOAD REDUCTION  NTG  Controlled phlebotomy  Atrial-to-femoral bypass OTHERS  Hypothermia  Soda Bicarb  Low minute ventilation THERAPEUTIC INTERVENTIONS  Anticipation of clamp removal is important.  Prior to clamp removal, increase preload. increasing the PCWP (if PAC used) by 3-4 mmHg above baseline  Discontinue agents such as NTG, nitroprusside & esmolol  Don‘t decrease anesthetic depth  Agents such as phenylephrine, ephedrine & epinephrine can be used  Raising BP 20-30% above baseline with such agents prior to clamp release is often necessary to avoid significant hypotension  Upon unclamping, acidic metabolites from the ischemic tissues below the clamp are washed back into the circulation  Prophylactic ventilatory adjustments to accommodate this increased acid load  Frequent ABGs
50  Renal protection strategies  buffer therapy with bicarbonate or THAM ( trisoaminomethane/tromethamine 0.3M)  After unclamping, reverse heparin  Discuss timing of reversal with surgeon.  ↓ Inhaled anesthetics  ↓ Vasodilators  ↑ Fluid administration  ↑ Vasoconstrictor drugs  Gradual release of clamp  Search for bleeding if ↓BP for more than 5min  Echo for cardiac function  Reapply cross-clamp for severe hypotension  Consider mannitol  Consider sodium bicarbonate Aortic cross clamp Passive recoil distal to clamp ↑catecholamines (& other vasoconstrictors) ↑ Impedance to aortic flow Active venoconstriction proximal & distal to clamp ↑ arterial resistance ↑ preload ↑coronary flow ↑contractility ↑Cardiac output↓ ↑ afterload If coronary flow & contractility increase If coronary flow & contractility do not increase
Aortic cross clamping Distal tissue ischemia Mediators release Distal vasodilation ↑ venous capacitance ↓ arterial resistance ↑ permeability (by end of clamping period) Unclamping Mediators production & washout ↓ myocardial contractility ↑ pulmonary vascular resistance Pulmonary edema Loss of intravascular fluid Central hypovolemia Distal shift of blood volume ↓ venous return ↓ cardiac output Hypotension
52 Mature vs immature Ach receptor NICOTINIC ACETYLCHOLINE RECEPTORS: (2α,β,δ,ε,), (2α,β,δ,γ )& (α7) MATURE IMMATURE Also called Junctional conventional Extrajunctional Fetal γ-subunit receptor Structure 2α,β,δ,ε 2α,β,δ,γ After muscle fibre injury; within 18hrs Fetus before innervations Burns Trauma Motor neuron lesion: upper or lower Insulin resistance state Sepsis Prolonged immobility Not seen in muscle protein catabolism & wasting that occurs with malnutrition Half life Approx 2w <24hrs Channel feature shorter open times and high-amplitude channel currents during depolarization Long open times and low-amplitude channel currents. Fast-gated, high-conductance channel type Smaller single channel conductance & 2- 10fold longer channel open time Significance 1. Increased sensitivity to depolarizing agents 2. Decreased sensitivity to non- depolarizing agent 3. Stays open for a longer time: thus increased efflux of intracellular potassium: can lead to lethal hyperkalemi Note: all this channel are insensitive to treatment with muscarinic acetylcholine receptor antagonist, atropine, but sensitive to treatment with α-bungarotoxin or muscle relaxants, which block the flow of current
Neuronal α7 AchR Muscular α7 AchR Choline do not open this Choline full agonist of muscle α7 AchR in conc. that do not open conventional AchR Readily desensitized. No desensitization occurs even in continued presence of choline allowing greater chance to efflux of K. Chemical α-conotoxin inhibits Does not get inhibited by α-conotoxin Methylcaconitine (selective antagonist of conventional α7 AchR) Muscular α7AchR also having low affinity for antagonist ( eg; pancuronium and α bungarotoxin), so high conc required. Conventional AchR antagonist bind with 1 α subunit whereas in these pentameric receptors 3 subunits are bind by an antagonist still 2 subunits available for binding to agonist and causing depolarization, resulting in resistance of α7AchR to blocking effect of drug. (eg: pancuronium)
54 Pattern of neuromuscular stimulation Feature ST TOF Tetanus DBS PTC Current strength Supramaximal Supra- or submaximal Supra- or submaximal Supra- or submaximal Supra- or submaximal Frequency 0.1–1 Hz 2 Hz four stimuli 30–50 Hz for 5 seconds Three impulses at 50 Hz repeated after 750 millisec 50 Hz for 5 seconds, 3 seconds later ST at 1 Hz Prerelaxant control Needed Not needed Not needed Not needed Not needed Pain on stimulation - -/+ ++ ++ ++ Sensitivity of manual detection (visual and tactile) Not sensitive Not sensitive at TOFR of 0.4 or more Sensitive Highly sensitive Sensitive Alteration of subsequent responses Not altered Not altered Altered (post- tetanic facilitation) Not altered Altered Interval between successive stimuli 5sec 12sec 2min 12-15sec 6min Receptor occupancy detection 75–90% 70–90% 70–90% 70–90% >90% Sensitivity for detection of subtle block Not sensitive Sensitive Sensitive Sensitive Not applicable Monitoring of profound block Not useful Not useful Not useful Not useful Useful
TOF vs double burst TOF-TRAIN OF FOUR STIMULATION DOUBLE BURST STIMULATION Four supramaximal stimuli given every 0.5sec(2Hz) Two short burst of 50Hz titanic stimuli of 60ms duration and 750ms apart. The number of impulse in each burst can vary: in DBS3,3 : 3impulses in each of two burst, in DBS3,2: the first burst 3impulse, the second 2 impulse. Introduced in early 1970 1989 Most frequently used Less frequent Introduced to : make clinically reliable throughout all phases without need of any objective monitoring device To improve tactile or visual evaluation(clinical evaluation) of recovery from neuromuscular blockade Degree of block can be read directly even though preoperative value is lacking Do Information of onset, degree & recovery all obtained Do Simple nerve stimulator Require special stimulator Less painful more Differentiate depolarizing block & non-depolarizing do Useful for detection of block in the range of surgical relaxation(70-100% receptor occupancy) do Does not influence subsequent monitoring of degree Doses influence( as this involve titanic stimulation): may potentiate subsequent response Fade is accurate only when TOF ratio <0.4 i.e when TOF ratio b/w 0.4-0.9 fade cannot be detected either visually or tactile. So subjective method overestimate recovery.Thus need of objective measurement. Tactile fade is better appreciated at higher TOF. But still not well appreciated at TOF 0.6-0.9, thus this also cannot replace objective monitoring. No Fade indicates 70-75% receptors blocked 60-70% receptors blocked Does not quantify intense block(i.e at no response to TOF) do Does not monitor phase I block of depolarizing block do
56 BIS vs Entropy BIS ENTROPY Principle Statistical analysis of frequency domain (power spectrum, beta ratio) & time domain (burst suppression ratio) Amount of disorder in a system. Irregular EEG→↑entropy →awake. Regular EEG→↓entropy →sleep. Value range 0-100 State entropy(SE): 0-91 Response entropy(RE): 0-100 SE-RE=0-3 Cortical/subcortical activity Cortical Cortical & subcortical. If RE>SE (>10)→↑musculoskeletal activity (subcortical) SE: cortical RE: subcortical Electrode 1,2,4,3 1,2,3 Interference with electrocautery More Less
Non depolarizing muscle relaxants: steroidal vs benzylisoquinolium vs Ether vs alkaloid NON-DEPOLARISING MUSCLE RELAXANTS STEROIDAL COMPOUNDS BENZYLISOQUINOLIUM COMPOUNDS PHENOLIC ETHER STRYCHNOS ALKALOID  Pancuronium  Pipecuronium  Vecuronium  Rocuronium  Ropacuronium(withdrawn bcoz of bronchoconstriction)  Gantacuronium(Shortest & fastest)  dTC(max histamine release)  Metocurine  Doxacurium(longest & most potent)  Cisatracurium  Atracurium  Mivacurium(shortest)  Gantacuronium(shortest & fastest under invest)  Gallamine(least potent)- nephrotoxic, teratogenic  Alcuronium high potency high potency long acting Long acting lack histamine release tendency to cause histamine release except doxacurium and cisatracurium - - vagolytic - strongly vagolytic Weak vagolytic hepatic Ester hydrolysis Hoffman elimination Not metabolized Not metabolized excreted by Kidneys Very less renal elimination, Only laudanosine (<30% excreted in kidney, 70% via bile) Excreted unchanged via kidneys Excreted unchanged in kidney Sugammadex can be used - - -
58 Scholine phase I vs phase II block COMPETITIVE BLOCK(D-TC) DEPOLARIZING (PHASE I) DEPOLARIZING (PHASE II) Paralysis in man Flaccid Fasciculations →flaccid Flaccid paralysis Paralysis in chick Flaccid Spastic Effect on isolated frogs rectus muscle No contraction, antagonism of ACh contractions Species sensitivity Rat > rabbit > cat Cat > rabbit > rat Human neonates More sensitive Relatively resistant Tetanic stimulation during partial block Poorly sustained contraction(fade) Well sustained contraction Unsustained(fade) Neostigmine Antagonises block No effect Antagonistic Post tetanic potentiation Present Absent Present Ether anaesthesia Synergistic No effect Order of paralysis Fingers, eyes → limbs → neck, face → trunk → respiratory Neck, limbs → face, jaw, eyes, pharynx → trunk → respiratory Effect of lowering temperature Reduces block Intensifies block Effect of cathodal current to end plate Lessens block Enhances block Structure-activity relationship: quaternary ammonium compounds similar to Ach Bulky rigid, do not activate muscarinic receptors More quaternary groups: longer acting, more potent Bridging structure between amines, lipohilic, determines potency Tertiary amine: histamine release Long thin flexible molecule: therefore has ganglionic, muscarinic effects End-plate membrane potential Depolarized to –55 mV Repolarization toward - 80 mV Onset Immediate Slow transition Dose-dependence Lower Usually higher or follows prolonged infusion Recovery Rapid More prolonged Mechanism Competitive blockade of Ach receptor Succinylcholine is comprised of two acetylcholine molecules joined together and acts as a depolarizing neuromuscular blocker by binding acetylcholine receptors at the post- synaptic neuromuscular junction end plate. The resultant end plate depolarization initially With increasing doses of succinylcholine (i.e., a large single dose, repeated doses, or a continuous infusion), a phase II block may occur. Continuous activation of acetylcholine receptors leads to ongoing shifts of sodium into the cell and potassium out of the cell.
stimulates muscle contraction; however, because succinylcholine is not degraded by acetylcholinesterase, it remains in the neuromuscular junction to cause continuous end plate depolarization and subsequent muscle relaxation. This is termed a phase I block. Despite this, the post- junctional membrane potential eventually moves in the direction of normal even in the continued presence of succinylcholine. This is due to increased activity of the sodium-potassium ATPase pump, which brings potassium into the cell in exchange for sodium. The receptor does not respond appropriately to acetylcholine, and neuromuscular blockade is prolonged. Phase II block may be seen clinically with doses of succinylcholine >4mg/kg, but some characteristics of this blockade have been reported at 0.3mg/kg. Also called dual, mixed, or desensitizing block Seen in pseudocholinesterase deficient people
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Atracurium vs Cis-atracurium ATRACURONIUM CIS-ATRACURONIUM  Non-depolarizing neuromuscular blocking agent  Intermediate duration of action  Benzylisoquinolinium compound  Undergoes temperature and pH-dependent chemical(Hofmann) degradation.  Degrades to form laudanosine and a monoquaternary acrylate: do not possess neuromuscular blocking activity  Metabolites eliminated by Urinary and hepatic pathways  Cholinergic receptor antagonist  Recovery index: 10-15min  No dosage adjustment required when use in geriatric patients and patients with renal/liver impairment  Suitable for continuous infusion  Minimal chances of prolonged recovery A racemic mixture of 10 steroisomers, of which 14% is cisatracurium A cis-isomer of atracurium- Bisbenzyltetrahydroisoquinolinium‖ One of ten stereoisomers in atracurium besylate Different isomer groups of atracurium have different pharmacokinetics, the trans-trans group having the highest clearance and the cis-cis group the lowest uniform 39% Organ-independent Hofmann elimination (77%) Undergo ester hydrolysis also Does not appear to be degraded directly by ester hydrolysis. Onset: 3-4min Intermediate time of onset ≥ atracurium and rocuronium. Onset: 4-6min - 3 times more potent than atracurium Atracuronium Metabolism minor pathway HYDROLYSIS by nonspecific esterases in blood quaternary alcohol + quaternary acid major pathway HOFFMANN elimination Laudanosine + quaternary monoacrylate 82% protein bound
62 0.25mg/kg ED95 :0.05mg/kg during N2O/O2/opioid Anesthetic 0.12mg/kg ED50:0.026mg/kg Time to max block: 3.2min 5.2 t1/2β: 22-25 mins (30-45 mins for 2X ED95 dose 0.1mg/kg) 0.5mg/kg Recommended intubating dose: 0.15-0.2mg/kg Duration: 35-45min Duration:40-50min Elimination t1/2: 17-21min Elimination half-life 22-35 min CVS effect: tachy, hypotension due to histamine release absent Histamine release present( immune mediated or chemical mediated) No histamine release (up to and including 8 x ED95) when administered over 5 to 10 seconds. Significant Laudonosine 1/3 to 1/10 of that produced with Atracurium Benzyl alcohol present The 10-mL multiple-dose vials of Cisa are contraindicated for use in premature infants • benzyl alcohol; (oxidized to benzoic acid, conjugated with glycine in liver & excreted as hippuric acid)metabolic pathway not well developed: gasping baby syndrome 0.5mg/kg 0.1mg/kg 5mcg/kg/min 10mcg/kg/min • Initial dose: 0.15mg/kg or 0.2mg/kg • Maintenance: 0.03mg/kg generally required 40– 50 minutes after initial dose • Infusion dose: 1–2mcg/kg/min • under opioid/nitrous oxide/oxygen anesthesia • Infusion in ICU: 3mcg/kg/min Lung protective(anti inflammatory action) Plasma clearance: 6.1-10.9ml/kg/min 5.2 Volume of distribution: 18-280ml/kg 31( follow 2compartment model) Commercial preparation: 10mg/cc 2mg/cc It is acidic: not compatible with alkaline solutions>8.5pH
Neostigmine versus sugammadex NEOSTIGMINE SUGAMMADEX CLASSIFICATION Anticholinesterase inhibitor Steroidal NDMR reversal agent CHEMISTRY 3-dimethylaminophenol derivative Cyclodextrin MOA By inhibiting anticholinesterase enzyme, it increases acetylcholine concentration at the synapse. Increased amount of acetycholine competitively reverse the action of NDMR. Envelops NMBA with high affinity binding & excreted in urine. Lipophilic inner core binds to Roc, Vec, Pan (in order of affinity). 1 molecule binds to 1molecule of NDMR. First neutralize NDMR present in plasma, then also dissociates NDMR at synapse. Duration of action Up to 4hrs Up to 24hrs Metabolism Slow hydrolysis by acetylcholinesterase & plasma esterases Not metabolized Elimination t1/2 50-90min 120min Vd 0.8lit/kg 11-14lit Clearance 1-16ml/min/kg 88ml/min Excretion 70% unchanged excreted in urine, 30% alcoholic metabolite excreted in urine Urine over 24hrs ADVANTAGES Cheap & easily available Rapid reversal(17times faster). When block is Shallow 2.2min(6.9min for neostig) Deep 2.7min (16.2min for neostig) Can be used for reversal of any type of NDMR Beneficial in obese ( in whom residual paralysis is hazardous eg. osa) Beneficial in elderly ( as they are prone for Postop pul comp) Other uses: myasthenia gravis, colonic pseudo-obstruction, snake bite, intrathecal additive for anesthesia, urine retention Rapid & predictable. So useful for airway rescue. Useful for any depth of blockade Makes rocuron useful in RSI, ECT and difficult airway(CICV) instead of suxamethonium Useful in myasthenia gravis for reversal , cardiac diseases to lessen side effects of neostigmine DISADVANTAGES Side effects: bradycardia, nausea, vomiting, abdominal crmps, diarrhoea, hypersalivation. Thus require co administration of anticholinergic (thus associated side effects too). Hypersensitivity & anaphylaxis: dose dependent Although can be sued for rocuron induced anaphylaxis Incidence is less compared to rocuron, neostigmine induced anaphylaxis. Dysgeusia, headache, fatigue, nausea, vomiting, dizziness Limited efficacy in reversing deep blockade Even though vecuronium can be reversed, it require twice the time of rocuron reversal (affinity for rocuron is 2.5times that of vecuron) Speed of recovery is unpredictable FDA approval for pediatric use is not available ( although it is safe, useful for airway rescue, similar dose as in adults) Ceiling effect when AChE inhibitors are Only useful for steroidal NDMR (note:
64 100% cysteine for novel isoquinoliniums, calabadion for all NDMR) Potentiate suxamethonium induced blockade Transiently increases aPTT & PT. (not significant at lower doses) Excess dose can itself lead to blockade like suxamethonium As exclusively excreted via kidneys, its safety not available in renal impairment patients. (Although sugammadex neutralize NDMR effect & not excretion of its complex in urine) Safety not available in pregnant women, breast feeding Patient using OCP will have contraception failure. So such patient should use backup methods like condoms. Co-administration with ondanset, verapamil & ranitidine lead to physical incompatability Cost & non availability Reversal when quantitative (objective) neuromuscular monitoring is available & reliable SUGAMMADEX no response to TOF PTC 0 16mg/kg PTC 1-15 4mg/kg TOF count 1-4 2mg/kg TOF<1 TOF<0.9 2mg/kg TOF> 0.9 NEOSTIGMINE TOF>0.9 TOF0.4- 0.9 0.02mg/kg TOF<0.4 or count 2-3 0.05mg/kg TOF 0-1 Delay reversal to TOF count of 2 No reversal
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Notes for Differences in Anesthesia

  • 1. 1 NOTES FOR DIFFERENCES IN ANAESTHESIA DR. RAVIKIRAN H M 2020 Ravikiran JAI JAWAN JAI KISAN
  • 2. 2 GURU KRUPA DR. RAVIKIRAN H M DNB POST GRADUATE STUDENT DEPARTMENT OF ANAESTHESIOLOGY KIDWAI MEMORIAL INSTITUTE OF ONCOLOGY BENGALOORU, KARNATAKA. WITH BLESSINGS OF MY GRANDPARENTS INSPIRED BY: DR. THAMEEM SAIF THANKS TO: MY FAMILY, SENIORS, FRIENDS & DEPARTMENT OF ANAESTHESIA, KIDWAI MEMORIAL INSTITUTE OF ONCOLOGY. Gmail: ravikiranhmkimmi@gmail.com
  • 3. INDEX SL. NO TOPIC PAGE RESPIRATORY SYSTEM 1. ODC vs CDC 12 2. CXR PA vs AP view 14 3. Respiratory failure types 15 4. Pulmonary edema: cardiogenic vs non cardiogenic 19 5. ARDS vs CHF vs Pneumonia 21 6. ARDS H vs L 22 7. Obstructive vs restrictive lung diseases PFT 23 8. Chronic bronchitis vs Emphysema 24 9. Chronic bronchitis vs small airways disease vs bronchiectasis 25 10. Lobar pneumonia vs Bronchopneumonia vs Interstitial pneumonia 26 11. DLT, Bronchial blockers: Advantage vs Disadvantages 27 12. Bronchial blockers 28 CVS 13. NTG vs SNP 30 14. Cardiac tamponade vs constrictive pericarditis 32 15. Constrictive pericarditis vs restrictive cardiomyopathy 33 16. Inotropes: Dopamine vs Dobutamine vs Adrenaline vs Noradrenaline 34 17. Meph vs Phenylephrine vs Ephidrine 41 18. Racemic adrenaline vs L adrenaline 43 19. Calcium gluconate vs calcium chloride 44 20. Type I vs Type II MI 45 21. Myocardial stunning vs myocardial hibernation vs infraction 46 22. Alpha stat vs pH stat 47 23. Aortic clamping vs unclamping 49 CNS AND NMJ 24. Mature vs immature Ach receptor 52 25. Pattern of neuromuscular stimulation 54 26. TOF vs double burst 55 27. BIS vs Entropy 56 28. Non depolarizing muscle relaxants: steroidal vs benzylisoquinolium vs Ether vs alkaloid 57 29. Scholine phase I vs phase II block 58 30. Atracurium vs Cis-atracurium 61 31. Neostigmine versus sugammadex 63 32. Myasthenia gravis vs Eaton-Lambert syndrome (Myasthenia syndrome) 65 33. Myasthenic crisis vs cholinergic crisis 67 34. Mannitol vs Hypertonic saline 68 35. Phenytoin vs Fosphenytoin 70 36. Head injury: SIADH vs Cerebral salt wasting vs diabetic inspidus 71 37. Carotid endarterectomy : GA vs RA, Premedication advantages vs disadvantages 72 38. CVA: THROMBOTIC vs EMBOLIC vs HEMORRHAGIC 73 HEPATICS 39. Types of Jaundice 74 40. HRS1 & 2 76 41. Hypoxia in cirrhosis: Portopulmonary HTN vs HPS vs cirrhotic hydrothorax 77 RENAL 42. Acute renal failure: Prerenal, renal vs post renal 78 43. RTA1, 2,3 & 4 79 44. Bartter vs Gitelman vs Liddle vs Conns 80 45. Hemodialysis vs hemoperfusion vs hemofiltration 81
  • 4. 4 46. IHD vs CRRT 83 47. Loop diuretics vs Thiazides vs Potassium sparing diuretics 84 48. Nephritic vs Nephrotic syndrome 86 49. Dailysis dementia vs Dialysis disequilibrium syndrome 87 ENDOCRINE 50. Type I DM vs Type II DM 88 51. Type I DM vs MODY 88 52. Dawns vs Somogyi phenomena 89 53. Tight vs classic non tight glycemic control of glucose 90 54. DKA vs HHS 92 55. Hyperthyroidism vs hypothyroidism clinical features 93 56. Thyroiditis:Hashimoto vs DeQueverians vs Reidles 94 HEMATOLOGY 57. Vit K antagonist versus Newer oral anticoagulants 95 58. Heparin vs low moleculae weight heparin vs Fondaparinaux 97 59. HIT 1 & 2 98 60. FFP, Cryo, Fibrinogen concentrate, PCC 99 61. Tranexamic acid vs EACA 100 62. Synthetic blood vs allogenic blood 101 63. Perflurocarbons vs Hb based oxygen carriers 102 64. Hemolytic transfusion reaction: acute vs delayed 104 65. TRALI vs TACO 105 OBSTRETICS 66. Jaundice in pregnancy: ICP vs HELLP vs AFLP 106 67. Thrombocytopenia with AKI D/D in pregnancy 107 68. Thrombocytopenia D/D in pregnancy 108 69. Choice of anaesthesia in PIH: GA vs RA 109 PEDIATRICS 70. Pediatric inhalational vs IV induction 110 71. Pediatric vs adult airway 112 72. Preterm vs term neonate 116 73. Children vs adults regional anesthesia 118 74. Uncuffed vs Cuffed ETT 121 75. Acute Epiglottitis vs Laryngotracheobronchitis 122 76. Omphalocele vs Gastroschisis 123 ENT & OPHTHALMOLOGY 77. Bronchoscope: Storz vs Negus 124 78. Foreign body airway removal: spontaneous vs controlled breathing 125 79. Retrobulbar vs Peribulbar block 126 BARIATRICS & ORTHOPEDICS 80. OSA vs OHS 128 81. Rheumatoid arthritis vs osteoarthritis 129 82. Ankylosing spondylitis vs ankylosis hyperostosis 131 83. Gout vs pseudo gout 132 GENERAL ANAESTHESIA 84. First order vs Zero order 133 85. Potency vs Efficacy 134 86. Types of hypersensitivity 135 87. Stages of Anesthesia 137 88. CO2 absorbents 138 89. Proseal versus I gel 139 90. Red rubber ETT vs PVC ETT 140 91. Pressurzing effect vs Pumping effect 141
  • 5. 92. Midazolam vs Remimazolam 142 93. Midazolam vs Lorazepam vs Diazepam vs Alprazolam 143 94. Barbiturates vs Benzodiazepines 145 95. N2O advantage vs disadvantage 146 96. N2O vs Xenon 148 97. Concentration vs second gas effect 150 98. Thiopentone vs Propofol vs Etomidate vs Ketamine 151 99. Halothane vs Isoflurane vs Sevoflurane vs Desflurane 157 100. Halothane hepatitis type 1 vs type2 161 101. Azeotrope: Halothane/Ether 162 102. Fentanyl vs Ramifentanil 163 103. Propofol vs Fospropofol 164 104. Crystalloids vs Colloids 165 105. NS vs RL 166 106. Colloids: Albumin, Dextran, Gelofusine, Hetastarch, Pentastarch 168 107. Clonidine vs Dexmedatomedine 170 108. Volume control vs pressure control vs pressure support 172 109. Flow trigger versus pressure trigger 174 110. Anaesthesia machine vs anaesthesia work station 175 111. Anesthesia & ICU ventilator 176 112. Yoke block vs yoke plug 177 113. NIST vs DISS 177 114. Direct vs indirect valves 178 115. Atropine, Glycopyrrolate & Hyoscine 179 116. Modified RSI: scholine vs Rocuronium 181 117. RSI: Modified RSI vs Protected RSI 182 118. Priming vs Precurarisation vs self taming 183 119. Serotonin syndrome vs Anticholinergic syndrome vs neuroleptic malignant hyperthermia vs malignant hyperthermia vs thyroid storm 185 120. MH vs AIR 187 121. Familial periodic paralysis hyperkalemic vs hypokalemic 189 122. Airway catheters: Bougie, Guides, AEC, Aintree, stylet 190 123. Respiratory complications during laparoscopy D/D 193 REGIONAL ANAESTHESIA 124. High frequency vs low frequency probe 194 125. Nerve locator vs peripheral nerve stimulator 195 126. Lignocaine, Bupivacaine, Levobupivacaine, Ropivacaine 196 127. Subdural vs Subarachanoid block 199 128. Epidural morphine versus fentanyl 200 129. Interpleural vs paravertebral block 201 130. RLB vs ESPB vs PVB vs TEA 204 ICU and CRITICAL CARE 131. HME filter Hygroscopic vs Hydrophobic 205 132. PEEP vs CPAP 206 133. Nasal cannula vs HFNO 207 134. Surgical tracheostomy vs Percut dilational tracheostomy 208 135. Antibiotics: time dependent vs concentration dependent 209 136. RBC cholinesterase versus pseudocholinesterase in OPCP 210 137. Cardioversion vs Defibrillation 211 138. Monophasic vs Biphasic 212 139. DPL vs E-FAST vs CT in abdominal trauma 213 PAIN & PALLIATION 140. Acute pain vs chronic pain 214
  • 6. 6 141. Nociceptive vs neuropthic pain 215 142. Slow pain vs fast pain 217 143. Somatic vs visceral pain 218 144. CRPS 1 vs CRPS 2 219 145. Neuralgia vs CRPS 220 146. Pain assessment : unidimensional vs multidimensional scales 221 147. Opioids : pure agonist vs mixed agonist/antagonist 222 148. Opioid induced Hyperalgsia: D/D 223 149. Tramadol vs tapentadol 224 150. Palliative care vs Hospice care 225 151. Head ache: Migrane vs Tension vs Cluster 227 152. Headache: Trigeminovascular cephalgias 228 153. Cryoneurolysis vs Peripheral nerve stimulation 229 154. Articular vs Nonarticular pain 230 STATISTICS 155. Standard deviation vs Variance vs coefficient of variation 231 156. Standard deviation vs Standard error 233 157. Sampling vs non-sampling errors 234 158. Point estimate vs confidence interval 235 159. Frequentist vs Bayesian statistics 236 160. Parametric vs non-parametric tests of significance 237 161. Sensitivity vs specificity 238 162. Cohort vs case control vs cross sectional study 239 163. Odds ratio vs likelihood ratio 241 164. Incidence vs Prevalence 242 165. Correlation vs regression analysis 243
  • 7. Contents ODC vs CDC...................................................................................................................................................................12 CXR PA vs AP view......................................................................................................................................................... 14 Respiratory failure types...............................................................................................................................................15 Pulmonary edema: cardiogenic vs non cardiogenic......................................................................................................19 ARDS vs CHF vs Pneumonia ..........................................................................................................................................21 ARDS H vs L...................................................................................................................................................................22 Obstructive vs restrictive lung ......................................................................................................................................23 Chronic bronchitis vs Emphysema................................................................................................................................ 24 CHRONIC BRONCHITIS vs SMALL AIRWAYS DISEASE vs ASTHMA vs BRONCHIECTASIS.................................................25 Lobar Pneumonia Vs Bronchopneumonia Vs Interstitial Pneumonia ..........................................................................26 DLT, Bronchial blockers: Advantage vs Disadvantages .................................................................................................27 Bronchial blockers ........................................................................................................................................................ 28 NTG vs SNP ...................................................................................................................................................................30 Cardiac tamponade vs constrictive pericarditis ............................................................................................................32 Constrictive pericarditis vs restrictive cardiomyopathy................................................................................................ 33 Inotropes: Dopamine vs Dobutamine vs Adrenaline vs Noradrenaline ........................................................................34 Meph vs Phenylephrine vs Ephidrine............................................................................................................................ 41 Racemic adrenaline vs L adrenaline.............................................................................................................................. 43 Calcium gluconate vs calcium chloride ......................................................................................................................... 44 Type I vs Type II MI ....................................................................................................................................................... 45 Myocardial stunning vs myocardial hibernation vs infraction ......................................................................................46 Alpha stat vs pH stat.....................................................................................................................................................47 Aortic clamping vs unclamping.....................................................................................................................................49 Mature vs immature Ach receptor ............................................................................................................................... 52 Pattern of neuromuscular stimulation.......................................................................................................................... 54 TOF vs double burst......................................................................................................................................................55 BIS vs Entropy ............................................................................................................................................................... 56 Non depolarizing muscle relaxants: steroidal vs benzylisoquinolium vs Ether vs alkaloid............................................57 Scholine phase I vs phase II block .................................................................................................................................58 Atracurium vs Cis-atracurium .......................................................................................................................................61 Neostigmine versus sugammadex ................................................................................................................................ 63 Myasthenia gravis vs Eaton-Lambert syndrome (Myasthenia syndrome) ....................................................................65 Myasthenic crisis vs cholinergic crisis ........................................................................................................................... 67 Mannitol vs Hypertonic saline ......................................................................................................................................68 Phenytoin vs Fosphenytoin...........................................................................................................................................70 Head injury: SIADH vs Cerebral salt wasting vs diabetic inspidus .................................................................................71 Carotid endarterectomy : GA vs RA, Premedication advantages vs disadvantages ......................................................72
  • 8. 8 CVA: THROMBOTIC vs EMBOLIC vs HEMORRHAGIC .....................................................................................................73 Types of Jaundice.......................................................................................................................................................... 74 HRS1 & 2.......................................................................................................................................................................76 Hypoxia in cirrhosis: Portopulmonary HTN vs HPS vs cirrhotic hydrothorax ................................................................ 77 Acute renal failure: Prerenal, renal vs post renal..........................................................................................................78 RTA1, 2,3 & 4................................................................................................................................................................ 79 Bartter vs Gitelman vs Liddle vs Conns ......................................................................................................................... 80 Hemodialysis vs hemoperfusion vs hemofiltration.......................................................................................................81 IHD vs CRRT ..................................................................................................................................................................83 Loop diuretics vs Thiazides ...........................................................................................................................................84 Nephritic vs Nephrotic syndrome.................................................................................................................................86 Dailysis dementia vs Dialysis disequilibrium syndrome ................................................................................................ 87 Type I vs Type II diabetes..............................................................................................................................................88 Type I vs MODY............................................................................................................................................................. 88 Dawn’s vs Somogyi phenomena ...................................................................................................................................89 Tight vs classic non tight glycemic control of glucose...................................................................................................90 DKA vs HHS ...................................................................................................................................................................92 Hyperthyroidism vs hyperthyroidism clinical features..................................................................................................93 Thyroiditis:Hashimoto vs DeQueverians vs Reidles ......................................................................................................94 Vit K antagonist versus newer oral anticoagulants.......................................................................................................95 Heparin vs low moleculae weight heparin vs Fondaparinaux....................................................................................... 97 HIT 1 & 2 Heparin induced thrombocytopenia .............................................................................................................98 FFP, Cryo, Fibrinigen concentrate, PCC......................................................................................................................... 99 Tranexamic acid vs EACA ............................................................................................................................................100 Synthetic blood vs allogenic blood .............................................................................................................................101 Perflurocarbons vs Hb based oxygen carriers.............................................................................................................102 Hemolytic transfusion reaction: acute vs delayed......................................................................................................104 TRALI vs TACO.............................................................................................................................................................105 Jaundice in pregnancy: ICP vs HELLP vs AFLP..............................................................................................................106 Thrombocytopenia + AKI in pregnancy D/D................................................................................................................107 Thrombocytopenia in preganancy D/d .......................................................................................................................108 Choice of anaesthesia in PIH: GA vs RA.......................................................................................................................109 Pediatric inhalational vs IV induction..........................................................................................................................110 Pediatric vs adult airway.............................................................................................................................................112 Preterm vs term neonate ...........................................................................................................................................116 Children and adults and implications for regional blocks ...........................................................................................118 UNCUFFED vs CUFFED ETT..........................................................................................................................................121
  • 9. Acute Epiglottitis vs Laryngotracheobronchitis..........................................................................................................122 Omphalocele vs Gastroschisis.....................................................................................................................................123 Bronchoscope: Storz vs Negus....................................................................................................................................124 Foreign body airway removal: spontaneous vs controlled breathing.........................................................................125 Retrobulbar vs Peribulbar block .................................................................................................................................126 OSA vs OHS.................................................................................................................................................................128 Rheumatoid arthritis vs osteoarthritis........................................................................................................................129 Ankylosing spondylitis vs Ankylosis hyperostosis .......................................................................................................131 Gout vs pseudogout....................................................................................................................................................132 First order vs Zero order kinetics ................................................................................................................................133 Potency vs Efficacy......................................................................................................................................................134 Types of hypersensitivity ............................................................................................................................................135 Stages of Anesthesia: Guedal......................................................................................................................................137 CO2 absorbents ..........................................................................................................................................................138 Proseal versus I gel .....................................................................................................................................................139 Red rubber ETT vs PVC ETT .........................................................................................................................................140 Pressurzing effect vs Pumping effect..........................................................................................................................141 Midazolam vs Remimazolam ......................................................................................................................................142 Midazolam vs Lorazepam vs Diazepam vs Alprazolam ...............................................................................................143 Barbiturates vs Benzodiazepines ................................................................................................................................145 N2O advantage vs disadvantage.................................................................................................................................146 N2O vs Xenon .............................................................................................................................................................148 Concentration vs second gas effect ............................................................................................................................150 Thiopentone vs Propofol vs Etomidate vs Ketamine ..................................................................................................151 Halothane vs Isoflurane vs Sevoflurane vs Desflurane ...............................................................................................157 Halothane hepatitis type 1 vs type2 ...........................................................................................................................161 Azeotrope: Halothane/Ether......................................................................................................................................162 Fentanyl vs Ramifentanil ............................................................................................................................................163 Propofol vs Fospropofol..............................................................................................................................................164 Crystalloids vs Colloids................................................................................................................................................165 NS vs RL ......................................................................................................................................................................166 Colloids: Albumin, Dextran, Gelofusine, Hetastarch, Pentastarch ..............................................................................168 Clonidine vs Dexmedatomedine.................................................................................................................................170 Volume control vs pressure control vs pressure support ...........................................................................................172 Flow trigger versus pressure trigger ...........................................................................................................................174 Anaesthesia machine vs anaesthesia work station.....................................................................................................175 Anesthesia & ICU ventilator........................................................................................................................................176 Yoke block vs yoke plug ..............................................................................................................................................177
  • 10. 10 NIST vs DISS ................................................................................................................................................................177 Direct vs indirect valves .............................................................................................................................................178 Atropine, Glycopyrrolate & Hyoscine .........................................................................................................................179 Modified RSI: scholine vs Rocuronium........................................................................................................................181 RSI: Modified RSI vs Protected RSI..............................................................................................................................182 Priming vs Precurarisation vs self taming ...................................................................................................................183 Serotonin syndrome vs Anticholinergic syndrome vs neuroleptic malignant hyperthermia vs malignant hyperthermia vs thyroid storm..........................................................................................................................................................185 MH vs AIR ...................................................................................................................................................................187 Familial periodic paralysis hyperkalemic vs hypokalemic...........................................................................................189 Airway catheters: Bougie, Guides, AEC, Aintree, Stylet ..............................................................................................190 Respiratory complications during laparoscopy D/D....................................................................................................193 High frequency vs low frequency probe .....................................................................................................................194 Nerve locator vs peripheral nerve stimulator.............................................................................................................195 Lignocaine, Bupivacaine, Levobupivacaine, Ropivacaine............................................................................................196 Subdural vs Subarachanoid block ...............................................................................................................................199 Epidural morphine versus fentanyl.............................................................................................................................200 Interpleural vs paravertebral block.............................................................................................................................201 RLB vs ESPB vs PVB vs TEA ..........................................................................................................................................204 HME filter Hygroscopic vs Hydrophobic .....................................................................................................................205 PEEP vs CPAP ..............................................................................................................................................................206 Nasal cannula vs HFNO...............................................................................................................................................207 Surgical tracheostomy vs Percut dilational tracheostomy..........................................................................................208 Antibiotics: time dependent vs concentration dependent .........................................................................................209 RBC cholinesterase versus pseudocholinesterase in OPCP.........................................................................................210 Cardioversion vs Defibrillation....................................................................................................................................211 Monophasic vs Biphasic..............................................................................................................................................212 DPL vs E-FAST vs CT in abdominal trauma ..................................................................................................................213 Acute pain vs chronic pain..........................................................................................................................................214 Nociceptive vs neuropthic pain ..................................................................................................................................215 Slow pain vs fast pain .................................................................................................................................................217 Somatic vs visceral pain ..............................................................................................................................................218 CRPS 1 vs CRPS 2.........................................................................................................................................................219 Neuralgia vs CRPS .......................................................................................................................................................220 Pain assessment : unidimensional vs multidimensional scales...................................................................................221 Opioids : pure agonist vs mixed agonist/antagonist...................................................................................................222 Opioid induced Hyperalgsia: D/D................................................................................................................................223
  • 11. Tramadol vs tapentadol..............................................................................................................................................224 Palliative care vs Hospice care....................................................................................................................................225 Head ache: Migrane vs Tension vs Cluster..................................................................................................................227 Headache: Trigeminovascular cephalgias ...................................................................................................................228 Cryoneurolysis vs Peripheral nerve stimulation..........................................................................................................229 Articular vs Nonarticular pain .....................................................................................................................................230 Standard deviation vs Variance vs coefficient of variation .........................................................................................231 Standard deviation vs Standard error.........................................................................................................................233 Sampling vs non-sampling errors................................................................................................................................234 Point estimate vs confidence interval.........................................................................................................................235 Frequentist vs Bayesian statistics ...............................................................................................................................236 Parametric vs non-parametric tests of significance....................................................................................................237 Sensitivity vs specificity ..............................................................................................................................................238 Cohort vs case control vs cross sectional study ..........................................................................................................239 Odds ratio vs likelihood ratio......................................................................................................................................241 Incidence vs Prevalence..............................................................................................................................................242 Correlation vs regression analysis...............................................................................................................................243
  • 12. 12 ODC vs CDC OXYGEN DISSOCITION CURVE CARBONDIOXIDE DISSOCIATION CURVE PaO2 versus SpO2 PaCO2 versus CO2 in blood Sigmoid shaped: becoz of co-operativity Linear, steep, left ward Thus increasing ventilation preferentially increase O2 content in blood in low V/Q ratio areas of lung Thus increasing ventilation CO2 excretion increases both in high & low V/Q ratios. Less soluble CO2 is 20times more soluble Less diffusible More diffusible Perfusion limited: have equal alveolar & pulmonary capillary partial pressure, so the amount of gas content transferred is dependent on blood flow. (however diffusion limited in pathological condition:  high cardiac output:↓ pulmonary transit time  high altitude: ↓PaO2  alveolar-capillary barrier disease: ↓ surface area, ↑ thickness) (thus transit time in pulmonary capillary decreased during exercise by 2/3 to 0.25sec will not affect in normal individuals, however cause exercise induced hypoxemia in pathological conditions) Note: N2O is also perfusion limited. Ventilation limited However as its more diffusible, in impaired diffusion capacity: oxygen is affected more than CO2, leading to type I resp failure. Note: Carbon monoxide is diffusion limited Diffusion limited: gases which fail to equilibrate i.e the partial pressure of a substance in alveolous does not equal that in pulmonary capillary. Thus Even small Shunt will effect Thus Shunt up to 50% will not effect Oxygen transported in blood: 2forms: bound Hb, dissolved CO2: 3forms: dissolved (10%), carbonic acid(68%), bound Hb-carbamino(22%). 98% in RBC 75% in RBC, 25% in plasma Doesn‘t follow. Only dissolved part follow. Follows Henry‘s law: number of molecules in solution is proportional to partial pressure at liquid surface.  Bohr effect: the O2 delivery to tissue increases when pH↓(CO2↑) i.e affinity of O2 to Hb↓.  This effects is not significant for O2 delivery at tissues.  Haldane effect: Release of CO2 from blood to lung occurs when O2 conc increases. I.e CO2 affinity for Hb decreases as O2 increases.  This effect is significant for CO2 elimination (contribute 50%). Factors affecting: temp, pH, CO2, 2,3DPG, amount & type of Hb, CO, isoflurane, propranolol Right shift: sickle cell, thalassemia Left shift: fetal hb, carboxyhb, methemoglobin, sulfhemoglobin O2 shift curve to right 4 important points:  Arterial point: pO2 100mmHg with SaO2 98%  Saturation fall off point: pO2 60mmHg with spO2 90%: determine critical for fall in SpO2  Mixed venous point: pO2 40mmHg with SaO2 75%: determine oxygen consumption  P50: pO2 26.6mmHg with SaO2 50%: determine shift of curve 2 points: Arterial point: PCO2 40mmHg Mixed venous point: PCO2 46mmHg
  • 14. 14 CXR PA vs AP view PA VIEW AP VIEW Scapula seen in periphery of thorax Scapula are over lung fields Clavicles are over lung fields Clavicles are above the apex of lung fields Posterior ribs are distinct Anterior ribs are distinct Heart is less magnified Heart is magnified Image is sharper Blurr Erect patient inspires more deeply showing more lung Ribs & clavicles are more horizontal Pleural air & fluid are more easy to detect on erect film
  • 15. Respiratory failure types RESPIRATORY FAILURE TYPE I TYPE II TYPE III TYPE IV AHRF(acute hypoxic respiratory failure) Lung failure Ventilator failure Pump failure Periop respiratory failure Shock PaO2:↓↓(<60mmHg) ↓ ↓ ↓ PaCO2: normal or ↓ ↑↑(>50mmHg)(pH<7.35) normal ↑ PAO2-PaO2 gradient: >30 normal Bicarb: normal Normal/raised(always raised in acute on chronic type II resp failure) Mechanism: ↑ shunt Inadequate alveolar ventilation atelectasis ↓ perfusion of respiratory muscle Causes: V/Q mismatch Low ambient oxygen(high altitude, hypoxic gas) Pulmonary embolism ILD:  Pulmonary oedema  Pulmonary haemorrhage  Hypersecretory pneumonia  Sarcoidosis  IPF: idiopathic pulmonary fibrosis Shunts: >30%  ARDS  Atelectasis  Pneumonia  R→L shunt cardiac disease Hypoventilation:  Neuromucular diseases Diaphragmatic paralysis Myasthenia crisis GBS Brainstem lesion obesity  Chest wall abnormalities Kyphosvoliosis Severe ankylosis spondylitis obesity Airway disease:↑Dead space becoz Alveolar vent=(TV-dead space)x RR  Acute severe asthma  Severe COPD Post surgical atelectasis  Increased atelectasis due to low FRC  Anaesthesia  Obesity  Ascitis  posture Circulatory failure: Shock ↓ ↓perfusion of chest muscle ↓ Fatigue ↓ Chest muscle failure (hypoventilation) Treatment: Oxygen therapy PEEP/CPAP Supportive ventilation Respiratory stimulants O2, Sedative & narcotics are beneficial Sedative & narcotics are hazardous Caution when giving O2(as O2 can worsen hypercapnia) 𝑷𝑨𝑶𝟐 = 𝑭𝒊𝑶𝟐 𝑷𝑩 − 𝑷𝑯𝟐𝑶 − 𝑷𝒂𝑪𝑶𝟐 𝑹 𝑃𝑎𝐶𝑂2 = 𝐾 × 𝑉𝐶𝑂2 (1 − 𝑉𝑑 𝑉𝑡 ) × 𝑉𝐴 where PAO2 = alveolar partial pressure of oxygen, FiO2 = fraction of inspired oxygen, PB = barometric pressure (760 mm Hg at sea level), PH2O = water vapor pressure (47 mm Hg), PaCO2 = partial pressure of carbon dioxide in the blood, and R = respiratory quotient, assumed to be 0.8. where PaCO2 = the partial pressure of carbon dioxide in the blood, K = constant, VCO2 = carbon dioxide production, Vd/Vt = dead space ratio of each tidal volume breath, and VA = minute ventilation. Hypoxemic respiratory Analysis of the previous
  • 16. 16 failure with a widened alveolar–arterial oxygen gradient is caused by V/Q mismatching or shunt pathophysiology. These two processes can be differentiated by improvement of the hypoxemia with supplemental oxygen, in the case of V/Q mismatch, and no improvement in cases with shunt. equation shows that hypercapnia can occur from three processes:  an increase in CO2 production, which is extremely uncommon clinically as a sole cause for hypercarbia,  a decrease in minute ventilation by either a reduced tidal volume or respiratory rate, and  an increase in dead-space ventilation Note: that hypoxia refers to an oxygen deficit at a tissue level and depends on oxygen delivery. Therefore, cellular hypoxia can be a result of any process that affects oxygen delivery to the tissues, and includes:  Hypoxic hypoxia  Anemic hypoxia  Circulatory hypoxia  Histotoxic hypoxia Oxygen Delivery = Cardiac Output × Arterial Oxygen Content DO2 = CO × CaO2 DO2 = CO × (1.39 × [Hb (g/dL)] × SaO2) + (0.003 × PaO2) Note: Mixed respiratory failure(pathophysiologic process that can contribute to both hypoxia & hypercapnia) Seen in acute on chronic respiratory failure conditions, CO poisoning Cyanide poisoning(hypoxic hypoxia) CO poisoning(anemic hypoxia, pulmonary edema) Anticholinesterase poisoning Cyanide poisoning( respiratory arrest) CO poisoning( respiratory depressant, airway obstruction)
  • 17. Hypoxemic respiratory failure Increased alveolar arterial gradient Normal alveolar arterial gradient Does PaO2 improve with supplement O2? Is PaCO2 elevated? Yes No V/Q mismatch Airway diseases  COPD, asthma, CF, BOS Interstitial lung disease  IPF, sarcoid, NSIP, DIP Alveolar filling  See list below Pulmonary vascular disease  Thromboembolism  Fat embolism Shunt Alveolar filling  Pulmonary edema  Left heart failure  Mitral valve disease  ALI/ARDS of any cause  Pneumonia  Trauma, contusion  Alveolar hemorrhage  Alveolar proteinosis  Drugs: heroin, paraquat  TRALI  Acute eosinophilic pneumonia  BOCP/COP  Aspiration  Upper airway obstruction  Near-drowning Atelectasis  Postoperative  Immobility Intrapulmonary vascular shunt  Pulmonary AVM  Hepatopulmonary syndrome Intracardiac shunt  PFO, ASD, VSD Yes No Hypoventilati- on (see below algorithm) High altitude low inspired PO2 ABBREVATIONS  CF: cystic fibrosis  BOS: bronchiolitis obliterans syndrome  IPF: interstitial pulmonary fibrosis  NSIP: nonspecific interstitial pneumonia  DIP: desquamative interstitial pneumonia  BOOP: bronchiolitis obiterans-organizing pneumonia  COP: cryptogenic organizing pneumonia  AVM: arteriovenous malformation
  • 18. 18 Hypercapnic respiratory failure Failure of one or more components of respiratory pump CNS Anterior horn cell Motor nerve Neuromuscular junction Muscle Airways & alveoli Excessive work of breathing  Drug effect (narcotics, sedatives)  Medullary stroke  Central apnea/hypoventilation syndrome  Metabolic alkalosis  Hypothyroidism  Idiopathic (Ondine‘s curse)  ALS/motor neuron disease  Poliomyelitis  Cervical spine injury  Guillian-Barre syndrome  Critical illness polyneuropathy  Fish toxin, tick paralysis, diphtheria toxin  Myasthenia gravis  Eaton-Lambert syndrome  Botulism  Organophosphate poisoning  Myopathy: drugs, steroids, infectious, critical illness, hypothyroidism  Muscular dystrophy  Polymyositis/dermatomyositis  Diaphragmatic dysfunction  COPD, asthma, cystic fibrosis  Pulmonary fibrosis  Pulmonary edema  Chest wall disorders, scoliosis  Obesity  Sepsis, metabolic acidosis  Upper airway obstruction  Tense ascitis, abdominal compartment syndrome
  • 19. Pulmonary edema: cardiogenic vs non cardiogenic CARDIOGENIC NON - CARDIOGENIC Types Flash Pulmonary Edema 1. ARDS 2. Re-expansion PE 3. High altitude PE 4. Reperfusion PE 5. Neurogenic PE 6. Drug induced PE Definition fluid transition from pulm cappilaries to interstitium and alveoli due to elevated pulm venous and left atrial pressures; without change in the permeability or integrity of the endothelial and epithelial layers of the pulmonary capillaries It is a manifestation of increased permeability of the pulmonary capillaries in which cardiac function is relatively preserved. Pulmonary artery wedge pressure ≤18 mmHg. Predisposing factor 1. LV systolic dysfunction 2. Diastolic dysfunction 3. Coronary heart disease 4. Hypertension 5. Valvular heart disease 6. Idiopathic dilated cardiomyopathy. 7. Toxins (e.g., anthracyclines) 8. Metabolic disorders (e.g., hypothyroidism) 9. Viral myocarditis (e.g., Coxsackie B virus or echovirus infection). 10. Chronic disorders : left ventricular hypertrophy of any etiology, hypertrophic and restrictive cardiomyopathies. 11. Acute causes : ischemia, acute hypertensive crisis 12. Left atreial or ventricular outflow obstruction - History & physical examiniation  H/o MI, CHF, valvular heart disease  S3 gallop, murmurs  Cold extrimities  Hypoxia – V/P mismatch – usually corrected by oxygen  H/o infections, aspiration, trauma, major surgeries, drug intake  Hypoxia – intrapulmonary shunt – not improved by oxygenation CXR  Cardiomegaly  Kerley B lines and loss of distinct vascular margins  Cephalization: engorgement of vasculature to the apices  Perihilar alveolar infiltrate  Pleural effusion  Vascular pedicle width >70mm  Heart size is normal  Uniform alveolar infiltrate  pleural effusion is uncommon  lack of cephalization  Vascular pedicle width <70mm Echocardiogram  Enlarged chamber  LV dysfunction present  Normal chamber size  No LV dysfunction Pulmonary Artery Catheterisation PAOP > 18 mmHg PAOP < 18 mmHg
  • 20. 20 Response to treatment Generally have an identifiable cause of acute LV failure—such as arrhythmia, ischemia/infarction, or myocardial decompensation that may be rapidly treated, with improvement in gas exchange. Usually resolves much less quickly, & most patients require mechanical ventilation. Treatment general principle:  Emergency management o Upright Sitting Posture o Support of oxygenation and ventilation  Oxygen therapy/positive pressure ventilation  Reduction of pre load & Inotrope support o Loop diuretics, Nitrates(NTG), Morphine  Conditions that complicate PE must be corrected o Infection, myocardial ischaemia, Renal failure, Anemia Reexpansion pulmonary edema  Diuretics and preload reduction are contraindicated, and intravascular volume repletion often is needed while supporting oxygenation and gas exchange. High altitude pulmonary edema  It can be prevented by use of dexamethasone, calcium channel– blocking drugs, or long-acting inhaled β2-adrenergic agonists.  Treatment includes descent from altitude, bed rest, oxygen, and, if feasible, inhaled nitric oxide; nifedipine may also be effective. HBOT.
  • 21. ARDS vs CHF vs Pneumonia Distinguishing factor ARDS CHF PNEUMONIA Symptoms Dyspnea + + + Hypoxia + + + Pleuritic chest pain +/- - + Sputum production +/- - + Tachypnea + + + Signs Edema - + - Fever +/- - + JVP raise - + - Rales + + + Third heart sound - + - Investigations B/L infiltrates + +/- +/- Cardiac enlargement - + - Elevated BNP +/- + - Hypoxemia + + + Localized infiltrate - - + PAO2/FiO2 ratioo <300 + - - PCWP <18mmHg + - + Response to Rx Antibiotics - - + Diuretics - + - Oxygen - + +
  • 22. 22 ARDS H vs L ARDS-Corona associated{CARDS}-Gattinoni’s dichotomanoius model H TYPE L TYPE High elastance(low compliance)-stiff lungs Low elastance(normal compliance) High lung weight Low lung weight High response to PEEP Low response to PEEP High recuritability Low recruitability High Right to left shunt Low ventilation perfusion ratio Baby lung( progression of L-type to H-type) Hypoxia due to Lungs lost HPV response, imbalance b/w angiotensin II & Angiotensin 1-7, pulmonary vascular thrombosis Rest of causes for ARDS & COVID-19(20-30%) Associated with COVID-19(70-80%) Most common form of ARDS(typical form) rare Require low TV & High PEEP for management Require high/normal TV and low PEEP PEEP beneficial PEEP harmful ?Antiinflammatory beneficial ?Anticoagulants beneficial
  • 23. Obstructive vs restrictive lung OBSTRUCTIVE RESTRICTIVE Airways Obstructed at any level from trachea to respiratory bronchiole Reduced expansion of lung parenchyma CXR Variable appearance depending upon the cause Typically bilateral infiltrates giving ground-glass shadows Examples • Chronic bronchitis • Emphysema • Bronchial asthma • Bronchiectasis • Chest cage disorders (e.g. kyphoscoliosis, poliomyelitis, severe obesity and pleural disease) • Interstitial lung diseases (ILDs) (e.g.pneumoconioses, idiopathic pulmonary fibrosis, immunologic lung diseases, collagen-vascular disease and sarcoidosis) PFT FEV1 ↓ ↓ FVC N ↓ FEV1/FVC ↓ N FRC ↑ ↓ TLC ↑ ↓ Raw ↑ N FEV25-75% ↓ N MBC ↓ N PEFR ↓ ↓
  • 24. 24 Chronic bronchitis vs Emphysema CHRONIC BRONCHITIS EMPHYSEMA Diagnosis Clinical: >3m cough for subsequent 2y Pathological: abnormal dilation of respiratory bronchioles & alveoli due to airflow obstruction Age 40-45y 50-75y Dyspnea Mid, late Severe, early Cough Early, before dyspnea Late, after dyspnea Sputum Copious, purulent Scanty, Appearance Blue bloater Pink puffer Infections common occasional Pathogenesis Impaired ciliary activity Deficiency of α1-antitrypsin Respiratory insufficiency repeated terminal PaCO2 50-60mmHg 35-40 PaO2 45-60 65-75 DLCO Normal to slight reduction Decreased Corpulmonale common Rare, terminal Airway resistance increased Normal or slightly increased Elastic recoil normal low CXR Prominent vessels, large heart Hyperinflation, small heart
  • 25. CHRONIC BRONCHITIS vs SMALL AIRWAYS DISEASE vs ASTHMA vs BRONCHIECTASIS CHRONIC BRONCHITIS SMALL AIRWAYS DISEASE ASTHMA BRONCHIECTASIS Location Bronchus(1-16th gen) Note: Brochus1-3 Bronchioles 4-19 Small airway 17-23 Bronchiole (17- 23rd gen) Bronchus Bronchus Age at diagnosis Adults Children Extrinsic: children Intrinsic: adults Adults Etiology Smoking, air pollution Viral infection, connective tissue disorder smoke Extrinsic: allergy Intrinsic: viral infection Infection, obstruction Pathogenesis Impaired ciliary Movement Damage to surfactant IgE-sensitised mast cells Damaged airways Major gross feature Thickened bronchial wall Occluded bronchioles Overdistended lungs Dilated bronchi and bronchioles Main histology Hyperplasia of mucous glands Fibrous plugs in bronchioles Mucus plugs in bronchioles Inflammed bronchi Major clinical feature Persistent cough with expectoration Cough, dyspnoea Bronchosplasm Copious foul-smelling expectoration
  • 26. 26 Lobar Pneumonia Vs Bronchopneumonia Vs Interstitial Pneumonia LOBAR PNEUMONIA BRONCHOPNEUMONIA INTERSTITIAL PNEUMONIA Definition Acute bacterial infection of a part of a lobe of one or both lungs, or the entire lobe/s Acute bacterial infection of the terminal bronchioles extending into adjoining alveoli. Also called lobular pneumonia Interstitium . Also called Hamman- Rich syndrome, Atypical pneumonia Age group More common in adults Commoner at extremes of age– infants and old age Commoner at extremes of age–infants and old age Predisposing factors More often affects healthy individuals Pre-existing diseases e.g. chronic debility, terminal illness, flu, measles immunocompramised Common etiologic agents Pneumococci, Klebsiella pneumoniae, Staphylococci, Streptococci Staphylococci, Streptococci, Pseudomonas, Haemophilus influenzae Viruses PJP Mycoplasma Chlamydia Pathologic features Typical case passes through stages of congestion (1-2 days) , early (2-4 days) and late consolidation (4-8 days), followed by resolution (1- 3 weeks) Patchy consolidation with central granularity, alveolar exudation, thickened septa Diffuse alveolar damage, interstitial edema composed of lymphocytes, type 2 pneumocyte Clinical features Consolidation features which is Unilateral, limited by anatomical boundaries Consolidation features with Bilateral, asymmetrical, not limited by anatomical boundaries Diffuse rales Investigations Neutrophilic leucocytosis, positive blood culture Neutrophilic leucocytosis, positive blood culture Lymphopenia, eosinophilia, HRCT CXR consolidation mottled focal opacities Diffuse hazy opacities, septal thickening USG consolidation Patchy B-lines, may show consolidation Patchy B-lines, may show consolidation Prognosis Better response to treatment, resolution common, prognosis good Response to treatment variable, organisation may occur, prognosis poor poor Complications Less common; pleural effusion, empyema, lung abscess, organisation Bronchiectasis may occur; other complications same as for lobar pneumonia fibrosis
  • 27. DLT, Bronchial blockers: Advantage vs Disadvantages ADVANTAGES DISADVANTAGES DLT Easy to place successfully Size selection more difficult Repositioning rarely required Difficult to place in patients with difficult airways or abnormal tracheas Bronchoscopy, Suction & CPAP to isolated lung is easily added Potential laryngeal trauma Can alternate OLV to either lung easily Potential bronchial trauma Placement still possible if bronchoscopy not available Not optimal for postoperative ventilation Best device for lung isolation BRONCHIAL BLOCKERS Easily added to regular ETT Positioning-more difficulty Difficult/abnormal airways Blind insertion less successful Children Right lung collapse difficult due to RUL anatomy Trachesotomised patient Displacement/repositioning more common, needs FOB Limited access to isolated lung-CPAP Limited access to isolated lung-min suction, bronchoscopy Accurate size not required Alternating isolation of lungs more difficult Allows ventilation during placement Selective lobar isolation possible Change of tube not required for postoperative ventilation
  • 28. 28 Bronchial blockers Cohen Blocker Arndt Blocker Fuji Uniblocker EZ-Blocker Size 9-Fr 5-Fr, 7-Fr, and 9-Fr 5-Fr, 9-Fr 7-Fr Balloon shape Spherical Spherical or elliptical Spherical Spherical × 2 Guidance mechanism Wheel device to deflect the tip Nylon wire loop that is coupled with the fiberoptic bronchoscope None, preshaped tip None Smallest recommended ETT for coaxial use 9-Fr (8.0 ETT) 5-Fr (4.5 ETT), 7-Fr (7.0 ETT), 9-Fr (8.0 ETT) 9-Fr (8.0 ETT) 7.5 ID Murphy eye Present Present in 9-Fr Not present No Center channel 1.6 mm ID 1.4 mm ID 2.0 mm ID 1.4 mm ID bronchial blocker has a high-volume, low- pressure cuff. bronchial blocker has a high-volume, low-pressure cuff. Y-shaped with the bifurcation of the main-stem into two distal extensions to be placed in both main-stem bronchus inner lumen contains a flexible nylon wire which exits as a small flexible wireloop. The wire loop is coupled with the fiberoptic bronchoscope and serves as a guide wire central lumens of both stems extend into the main shaft and with ports to suck out secretions or CPAP Once inserted repositioning very difficult as wire guidance not possible
  • 30. 30 NTG vs SNP NTG SNP Chemistry Organic Inorganic: five CN and one NO combined Preparation Oral, SL, Patch & Injectable Injectable Injectable available as Solution Powder form-to be reconstituted. Protect from light & use in 12hrs. Stability Absorbed by some plastic(upto80%) Stored in glass vials Unstable in light & alkali. Stored out of light: alumini foil MOA NTG+Endothelium→N2O→NO Via gluthione S-transferase SNP+Hb→Methemoglobin+CN+NO NO act on SH group of smooth muscle → stimulate cGMP by ↑ Guanyl cyclase enzyme→smooth muscle relaxation. NO released by enzymatic nteraction NO released spontaneously(non enzymatic activation) Systemic action  At low doses Venous>arterial (selective): so preload reduction  Thus disrupts renal autoregulation  Bronchodilation, Pul, Vasodilation→↑shunt  ↑ICP  Antiplatlet action  Used in angina  Act equally on veins & arteries (non selective) so no regional effect. Both preload & after load reduction.  Thus renal blood flow maintained  Attenuates HPV→↑Shunt  ↑ICP becoz of ↑CBF: only in early stage Pharmaacokinetics: Absorption  Very high first pass metabolism(upto 95%)  Rapid aabsorption via other routes  Only IV preparation Distribution Large-60% protein bound Not known Metabolism Hepatic→Thiols Rapid liver rhodanase→ prussic acid→ thiocyanate (eliminated in 3-7days) Elimination 2-4min via urine 2-4min via urine Side effects Hypotension with tachycardia Tolerance Methemaglobin(so ↓O2 carrying capacity) Hypotension with tachycardia No tolerance Becoz of thiocyanite Nausea, vomiting, pain abdomen, hypereflexia, seizure Rebound HTN Long term: cyanide toxicity methemoglobin Coronary steal Coronary blood flow MI - ↑ ↓ + ↓ ↑ Cardiac output ↓↑ ↑ MAP ↓ ↓↓ SVR ↑ ↓ Pul VR ↓ ↓↓
  • 31. Head ache + - Dose 5-50mcg/min Toxicity:  For siginificant methemoglobinemia: 250mcg/min for 7days 0.2-10mcg/kg/min Toxicity:  For cyanide toxicity:  Not more than 0.5mg/kg/hr or 2mcg/kg/min. Plasma CN conc to be < 3µmol/l.  For thiocyanate toxicity: 2- 5mcg/kg/min for 7-14days.  For 10% methemoglobin formation 10mg/kg.
  • 32. 32 Cardiac tamponade vs constrictive pericarditis CARDIAC TAMPONADE CONSTRICTIVE PERICARDITIS After systole here slow expansion ↓ So gradual descent of y After systole its fast ↓ So pericardial knock & rapid y descent - Rapid y descent[PAY TAX] Rapid x descent [PAY TAX] +/- Kussmaul sign: absent [becoz pericardium can still expand] Present [normally JVP fall during inspiration as negative pressure in mediastinum. In constrictive pericarditis no effect of inspiration leading to negative pressure change in pericardium, so JVP rise during inspiration] Pulsus paradox: +++. Inspiration → RV dilation → pressure in pericardial fluid ↑ → LV pushed in → ↓ LV filling→↓SBP. + Inspiration→ RV dilation → septum move to LV →↓LV filling→↓SBP. Equalisation of diastolic pressure:+ + Becks triad[hypotension, rised JVP, muffled heart sounds], Moschcowitz triad[widening of cardiac flatness, abrupt transition from pulmonary to cardiac flatness, wiening of cardiac dullness in second intercostals space], ECG triad[S tachy, Low voltage, electrical alternans), POCUS triad[pericardial fluid, RV diastolic collapse, dilated IVC] Triad of pericardial knock, raised JVP, retractile apex in the setting TB - Pericardial knock Low voltage ECG: ++ Electrical alternans:++ ++ - Apex not identifiable Retractile apex - Square root/dip & plateau sign in diastolic waveform Acute/chronic chronic Treatment: pericardiocentasis Pericardial stripping
  • 33. Constrictive pericarditis vs restrictive cardiomyopathy CONSTRICTIVE PERICARDITIS RESTRICTIVE CARDIOMYOPATHY HFpEF HFpEF Pericardial Diastolic heart failure Myocardial Diastolic heart failure JVP: raised raised Square root/dip & plateau sign in diastolic waveform: frequent Square root/dip & plateau sign in diastolic waveform: rare Equalisation of pressure: frequent Rare(usually L>R) Kussmaul sign: present present chronic chronic Predominant right sided heart failure Right &/ or left Prominent y descent Variable y descent Pulsus paradox: usually absent rare - Conduction abnormality : common Idiopathic, following Sx, RT Primary or infiltrative, drug, RT History of pericarditis(peluritic chest pain, fever, cardiac surgery, trauma, RT, connective tissue disorder): + - Dissociation of intrathoraxic & intracardiac pressure: discordant Rt & Lt ventricle peak systolic pressures Are in phase Enhanced ventricular interdependence: movement towards left ventricle on inspiration little Pericardial knock Third heart sound MR, TR: absent Present often On Echo: E‘: normal or increased Decreased( ventricular speckling in amyloidosis) MRI/CT: pericardial thickening - Endomyocardial biopsy: not useful useful Treated with pericardiectomy, anti-inflammatory Conservative, stem cell transplant, cardiac transplant Prognosis: good poor ANESTHESIS MANAGEMENT: also same for cardiac tamponade  Positive pressure ventilation is dangerous( decrease venous return)  Avoid decrease in HR, cardiac contractility, SVR(thus ketamine is useful) AF is dangerous
  • 34. 34 Inotropes: Dopamine vs Dobutamine vs Adrenaline vs Noradrenaline DOPAMINE DOBUTAMINE ADRENALINE NORADRENALINE Preparation Clear, colorless solution for injection containing 40mg/ml of dopamine hydrochloride  Vials containing 250mg of dobutamine hydrochloride and 250mg mannitol in a lyophilised form.  It is also available as 20 ml vial containing 250mg of dobutamine hydrochloride (12.5mg/ml) with 4-8 mg of sodium bisulphite dissolved in water.  50mg/ml 5ml ampoule  Clear solution for injection containing 1mg/ml of adrenaline hydrochloride.  Also comes as aerosol spray delivering 280 μg metered dose of adrenaline acid tartrate. As a clear colourless solution for injection containing 2 mg/ml of noradrenaline acid tartrate Chemical origin Catecholamine synthetic isoprenaline derivative catecholamine catecholamine t1/2 1min 2.4min 2min 3min Dose  Renal dose 0.5-2 μg/kg/min  β1 action 2-10 μg/kg/min  α & β1 action 10-20 μg/kg/min  endogenous noradrenaline release at dose >5 μg/kg/min 2.5 - 10 μg/kg/min ; occasionally upto 40 μg/kg/min Pressor support  1–2 μg/min predominantly activates β2 receptors leading to vascular and bronchial smooth muscle relaxation  2 – 10 μg/min β1 and β2 action. Heart rate,contractility and conduction through AV node increased.  >10 μg/min marked α stimulation and generalized vasoconstrictions CPR  1 mg (ie 0.02 mg/kg) IV stat is given for asystole, VF  In situations where IV access is not available adrenaline 0.01- 0.5 μg/kg/min.
  • 35. dose is tripled and diluted in 10 ml saline, to be given via endotracheal tube or intraosseous route. Bronchodilation:-  Due to its vasoconstrictive action adrenaline is used to reduce airway obstruction caused by oedematous mucosa in patients of severe croup, post extubation & traumatic airway edema.  Adrenaline is used for nebulization in such patients. Effect of each nebulisation lasts for around half to one hour. 0.05ml/kg(max 1.5cc) diluted to 5cc with NS.  Subcutaneous injection of adrenaline is also used for this purpose. Dose is 300μg (1/3rd ampoule) every 20 minutes. Upto 3 such doses can be given. Mechanism of action Has 2 mechanisms of action one is via direct stimulation of receptors and second is via indirect release of noradrenaline Direct Action:-  Low doses:- It stimulates dopaminergic receptors D1 and D2  D1 causes mesenteric and renal bed Predominantly β adrenergic receptor stimulating agent (β1 > β2>α)  At lower doses it causes β stimulation.  At higher doses α stimulation predominates.  The drug causes β mediated rennin release. This indirectly potentiates the vasoconstrictor action.  This drug exerts its action predominantly at α – adrenergic receptors, with a minor action on beta receptors.  Noradrenaline when given exogenously (ie. Via intravenous route) can produce bradycardia while endogenous release of the drug evokes
  • 36. 36 vasodilatation  β action begins at around 3μg/kg/min  Beyond 10 μg/kg/min α action predominates Indirect Action:- Its indirect action is via release of noradrenaline. This action begins at a dose of 5μg/kg/min. Prolonged use of dopamine causes depletion of noradrenaline stores and decreased response to the drug. tachycardia. HEART  Produces positive inotropic effect by stimulating β1 receptors.  Heart rate is increased due to positive chronotropy  Force of cardiac contraction (positive inotropism) is increased via direct β1 action.  Afterload is decreased due to β2 mediated fall in peripheral vascular resistance.  Increase in cardiac contractility along with fall in afterload causes improvement in CHF patients.  Left ventricular end diastolic volume reduces and organ perfusion improves.  It has both positive inotropic and positive chronotropic effect on heart.  As a result myocardial oxygen demand is also increased.  It is the drug of choice at the end of cardiopulmonary bypass when maximal inotropic effect is required.  Conduction through AV node improves and AV block if present is reduced.  It causes increase in peripheral vascular resistance leading to rise in blood pressure.  Cardiac output remains unchanged or decreases slightly as heart has to work against increased afterload.  This also results into increased myocardial oxygen demand. QT prolongation: + + + + Blood vessels  E ndogenous norepinephrine release produced by dopamine causes considerable vasoconstriction.  Moreover this  Vasodilation occurs due to β2 action on blood vessels.  At lower doses β mediated vasodilation.  While at higher doses vasoconstriction predominates leading to increase  It causes α mediated increase in peripheral vascular resistance leading to increase in blood pressure.
  • 37. drug has no major action on β2 receptors and therefore unopposed stimulation of α1 receptors is responsible for overall vasoconstriction.  At low doses D1 mediated splanchnic & renal vasodilation occurs. in SVR RS  Ventilatory response to hypercapnia and hypoxia is reduced by dopamine due to action on dopaminergic receptor located in the carotid bodies (Peripheral chemo receptors).  Increases pulmonary artery pressure -  It is a respiratory stimulant though this action is not very significant clinically.  It is a potent bronchodilator due to βaction.  It reduces vocal cord edema in patients of croup α1 mediated vasoconstriction. It causes slight increase in minute volume along with some degree of bronchodilatation CNS  Probably causes vasodilation of normal cerebral vasculature with no effect on CMR.  Very high dose may cause cerebral vasoconstriction.  Exogenous dopamine does not cross BBB except in its levo-rotatory form.  It also stimulates CTZ leading to nausea.  Increases CMR and cerebral blood flow at high doses.  No or minimal effect is seen in low doses.  BBB defect exaggerates the phenomenon.  It penetrates CNS to a limited extent.  CMR & CBF are increased especially when BBB is open.  It does not have much effect on CBF & CMR when BBB is intact.  Cerebral vasodilation & increase in CMR occurs when BBB is open. Kidney  At low doses causes marked  Increase in cardiac output  RBF is reduced by 40%, although GFR ↓RBF
  • 38. 38 renal vasodilatation leading to corresponding ↑RBF  Increase in urine output is also due to interference with renal tubular function.  At higher doses vasoconstriction predominates and the advantage on RBF is lost. causes increase in urine output.  Specific action on RBF is absent. may remain minimally altered.  Increase in sphincter tone and decrease in bladder tone may cause difficulty in micturition. GIT Splanchnic blood flow is increased due to action on DA1 receptors.  Total increase in cardiac output improves organ perfusion.  Direct action on gastrointestinal vasculature is not present.  Intestinal tone & secretions are decreased.  Splanchnic blood flow is increased when used in β dose  Vasoconstriction predominates at higher doses. Hepatic & splanchnic blood flows are decreased. Pregnant uterus Inhibits contractions of pregnant uterus. Increases contractility of the pregnant uterus, may cause fetal bradycardia & asphyxia. Metabolic & other effects Release of prolactin, growth hormone & aldosterone are depressed. -  ↓ insulin secretion.  Glucagon secretion is ↑ resulting into rapid glycogenolysis & raised blood sugar levels.  ↑ in activity of lipases causes increased concentration of FFA (free fatty acids) in blood.  BMR ↑ by 20 – 30%  Renin activity is ↑ in plasma.  Decreases insulin secretion leading to hyperglycemia.  Plasma rennin activity rises.  FFA concentration is ↑
  • 39. Pharmacoki netics  One fourth of the administered dose is converted to noradrenaline within adrenergic nerve endings.  Metabolites are excreted in urine either as such or after glucuronide conjugation. Also excreted in feces Natural endogenous catecholamine Synthetic derivative Natural endogenous catecholamine Natural endogenous catecholamine Nonchiral compound Two isomers present: L(–) and R(+) Two isomer Vd 1.8–2.5 l/kg 0.2 l/kg Side-effects Raise blood sugar Raised IOP Nausea & vomiting Potentiates development of MODS Reduce blood sugar Allergy present Contraindic ations Pulmonary HTN, cor pulmonale Aortic stenosis, mitral stenosis Shock  Cardiogenic without arrhythmia  Cardiogenic SBP 70-90  Cardiogenic with SBP>90  Pulmonary embolism, cor pulmonale  CPR  Cardiogenic(2nd line)  Septic(2nd choice)  Anahylactic  neorogenic  Cardiogenic with arrhytmia  Cardiogenic SBP<70  septic α 1 ++ + +++ +++ α 2 + - ++ +++ β 1 ++ +++ +++ + β 2 +++ + ++ - D +++ - - - Inotrope+vasopresso r inodilator Inotrope+vasopressor Inotrope+vasopressor HR + + ++ - MAP ++ + + +++ Dopamine ↓ ↓ Homovanilic acid ↓ 3,4 dihydroxy phenyl acetic acid MAO & COMT Dobutamine ↓ ↓ 3-Omethyl dobutamine (inactive) ↓ Glucuronide conjugation ↓ Excreted in urine mainly COMT Adrenaline ↓ ↓ Metadrenaline & normetadrenaline ↓ 3 methoxy 4 hydroxyphenyl ethylene + 3 methoxy 4 hydroxy mandelic acid ↓ Excreted predominantly in urine COMT Noradrenaline ↓ ↓ Methylation & oxidative deamination of compound ↓ VMA Predominant metabolie; Excreted in urine (3 methoxy, 4 hydroxy mandelic acid) MAO & COMT
  • 40. 40 SVR + - +/- +++ Inotropy ++ ++ ++ + CO +++ +++ ++ +/- Arrhythmia ++ + ++ + Increased myocardial O2 demand + - + + Main harmone of adrenal medulla Main neurotransmitter of sympathetic system
  • 41. Meph vs Phenylephrine vs Ephidrine VASOPRESSORS SYNTHETIC NONCATECHOLAMINES SYMPATHOMIMETICS PHENYLEPHRINE EPHEDRINE MEPHENTERAMINE MOA Selective α1 receptor agonist at clinical doses, increasing systemic vascular resistance secondary to vasoconstriction. Primarily causes venoconstriction.  α and β receptor agonist.  Both direct and indirectly acting , clinical effect is primarily due to its indirect action of releasing norepinephrine from postganglionic nerve endings  α and β receptor agonist.  Both direct and indirectly acting ADVANTAGES  Immediate onset  short duration of action 10-15 minutes  Ideal for continuous infusion  Economical  Does not need multiple dilutions as compared to Phenylephrine.  No bradycardia  Economical  Does not need multiple dilutions as compared to Phenylephrine ,  immediate onset of action peaking at 5 min and lasting 15-30 min DISADVANTAGES  Tachyphylaxis.  Reflex bradycardia and  serial dilution for IV administration is source of error  genetic polymorphism lead to variable response  Tachyphylaxis.  Tachycardia,  Adverse effect on fetal acid base status  as compared to Phenylephrine delayed onset of action,  longer duration of action of about 60 min  attenuated response with cocaine, reserpine  accentuated response in patient on MOA inhibitors  Tachyphylaxis.  Little evidence available on placental transfer and its foetal metabolic impact IV Preparation 10mg/ml 50mg/ml 30mg/ml Other actions  Particularly useful in patients with coronary artery disease and in patients with aortic stenosis because it increases coronary perfusion pressure without chronotropic side effects, unlike most other.  Nasal spray is a 1% solution for decongestion  chronic oral medication to treat bronchial asthma  acute coryza  0.5 mg/kg intramuscularly, has an antiemetic effect  Nasal decongestant  Stimulant in psychiatry
  • 42. 42 CNS stimulation is minimal Causes hyperkalemia (opposite of beta action) Mydriasis accompanies the administration of ephedrine, and CNS stimulation does occur CNS stimulant Duration of action 15min 60min 30min F/M Ratio 0.17 0.71 Metabolism MAO deaminated by MAO in the liver, and hepatic conjugation also occurs. The slow inactivation and excretion of ephedrine are responsible for the prolonged duration of action n-demethyation in liver microsome Elimination <0.5% excreted unchanged in urine 40% excreted unchanged in urine urine Bolus dose 50-200mcgIV 5-10mg IV 3-6mg IV Infusion 20-100mcg/min - -
  • 43. Racemic adrenaline vs L adrenaline RACEMIC ADRENALINE L-ADRENALINE Strength: 2.25% i.e 22.5mg/ml 0.1% [1:1000] i.e 1mg/ml Contain both L & D form @ 1: 1 ratio L-form is most active Not available in India(available only in USA) Readily available Was preferred for nebulisation over more active & more readily available l-epinephrine to minimize anticipated CVS side effects such as tachycardia & HTN Can be used. Found to be equally effective & does not carry risk of additional adverse effect Dose for nebulisation: 0.05ml/kg(max of 0.5ml i.e 11.25mg) of 2.25% solution with 2.5ml NS 0.5ml/kg (max of 5ml i.e 5mg) of 1:1000 solution with 4-5ml NS Costly Less expensive
  • 44. 44 Calcium gluconate vs calcium chloride CALCIUM CHLORIDE CACIUM GLUCONATE Elemental calcium content: 13.6mEq/gm of Calcium (3times more potent) 4.65mEq/gm 1gm/10ml: 10% 1gm/10ml: 10% Osmolarity: 2000mOsm/l 680mOsm/l Available calcium: 27.2% 9.3% Preferred administration via central line Peripheral administration Can cause tissue necrosis Risk of tissue necrosis & phlebitis is less Dilute (20mg/ml) & administer at slower rate 1gm over 10min Can be given slow IV push Preferred in cardiac arrest & poor liver function. However 1/3rd of dose is used. Require hepatic metabolism for removal of gluconate and formation of active Ca 2+ . So in setting of poor liver function & cardiac arrest (emergency) it is not preferred.
  • 45. Type I vs Type II MI TYPE I TYPE II Acute atherothrombotic coronary event Acute imbalance between oxygen supply (eg. Hypoxemia, anemia, hypotension, vasospasm ) and demand (eg. Tachycardia, anemia, hypertension, surgical stress). No coronary artery disease. Chest pain more common symptom Dyspnea Initial presentation suggestive of MI Non cardiac problem (sepsis, trauma, hemorrhage) Amount of clinical stress low High (high dose vasopressors, anemia, hypoxemia, hypotension) STEMI or NSTEMI ST depression Echo : new RWMA, reduced EF Hyperkinetic, underfilled heart Troponin elevation: more Moderate Evidence based treatment established no Reperfusion strategy (invasive), anticoagulants Frequently managed non-invasively & received less frequently cardio-protective drugs Treat underlying cause Note: Type 3: sudden unexpected cardiac death often with symptoms suggestive of myocardial ischemia Type 4: associated with percutaneous coronary intervention or stent thrombosis Type 5 : associated with cardiac surgery MINS: myocardial injury after noncardiac surgery. Troponin elevation apparently from cardiac ischemia with or without signs, symptoms and ECG changes.
  • 46. 46 Myocardial stunning vs myocardial hibernation vs infraction MYOCARDIUM STUNNING HIBERNATION INFRACTION Regional dysfunction + + + Tissue perfusion Uncoupling (flow normal, muscle function ↓) Coupling (flow ↓, muscle function ↓) Coupling (flow -, muscle function-) pathogenesis Relief of ischemia: transient post ischemic dysfunction Persistent ischemia(survival hypothesis), repetitive stunning hypothesis, smart heart hypothesis Necrosis, scarring Onset Sudden following ischemia and reperfusion event: stress/CABG/stent After weeks or months of ischemia Acute: thrombotic Chronic: stenotic Resolution 6-8hrs post CPB Delayed, days to months following revascularisation absent Inotropic support Has effect on stunned myocardium Has effect No effect Revascularisation Beneficial beneficial Not beneficial PET scan/ MRI Viable viable Non viable
  • 47. Alpha stat vs pH stat ALPHA STAT METHOD pH STAT METHOD It considers the alkaline pH seen during CPB is physiological (increased solubility of carbon dioxide seen during hypothermia raises the pH.) pH & Pco2 are maintained at normal values regardless of the body temperature. no additional measures to correct the pH/ PCO2 levels are undertaken. In order to maintain PCO2, CO2 is added to the ventilating gas mixture. more commonly used method This method is not preferred preserve cerebral autoregulation & improve myocardial preservation. patients tend to have higher CBF because of increase in CO2 content and there will be loss of cerebral auto regulation. More flow, more chances of micro- embolization. Blood pH : alkalotic Normal Intracellular pH : normal acidotic Intracellular enzyme function: maintained decreased Technically demanding: no Yes[require adding of CO2] Total CO2 content kept constant [pH & pCO2 vary with temp] pH kept constant Advantage 1. Better enzyme function 2. ↓CBF coupled with ↓energy 3. Coupling independent of cerebral perfusion pressure 4. Less arryhythmia 5. Better cerebral recovery 6. ↓microemboli Advantage 1. ↑CBF global cerebral cooling (↓O2 consumption) 2. Better flow to deep brain structure Better in adults [less stroke] Better in children [good oxygenation] Disadvantage • ↓CBF Disadvantage • Brain injury↑: because 1. ↑micremboli 2. ↑ICP 3. Cerebral edema 4. Steal phenomena 5. Abolition of cerebral autoregulation 6. Redistribution away from marginally per fused area
  • 48. 48  PaO2 ↓ by 5mmHg for each degree below 37 0 C  PaCO2 ↓ by 2mmHg for each degree below 37 0 C  Change in pH=0.015pH units/degree change in temp  However electrical neutrality has to be maintained, so protein like histidine imidazole play role in maintaining it. Alpha = unprotinated histidine imidazole / [H+ ] Variable +1 o C -1 o C pH -0.015 +0.015 pCO2 +0.27kPa (2mmHg) -0.27kPa (2mmHg) pO2 +0.6kPa (5mmHg) -0.6kPa (5mmHg) Combination of alpha & pH stat: Goal: maintain constant pH during cooling & restore electrochemical neutrality before circulatory arrest. Method: Use temperature corrected values during cooling & rewarming. Temperature uncorrected values in between. CO2 initially increases during cooling. Advantage: produce homogenous brain cooling, then restore neutrality, improves CMRO2. During CPB Hypothermia for organ protection @20 0 C CO2 solubility ↑ ↓PaCO2 [as temp↓→solubility ↑→pressure↓] @ 37 0 C CO2 solubility ↓ ↑PaCO2 @20 0 C H2O→H+ + OH- Reaction is inhibited So H+ ↓and pH ↑ @ 37 0 C H2O→H+ + OH- Promoted So H+↑ and pH↓
  • 49. Aortic clamping vs unclamping AORTIC CROSS CLAMPING AORTIC UNCLAMPING HEMODYNAMIC CHANGES  ↑ Arterial BP above the clamp  ↓ Arterial BP below the clamp  ↑ Segmental wall motion abnormalities  ↑ Left ventricular wall tension  ↓ Ejection fraction  ↓ Cardiac output  ↓ Renal blood flow  ↑ Pulmonary occlusion pressure  ↑ CVP  ↑ Coronary blood flow HEMODYNAMIC CHANGES  ↓ Myocardial contractility  ↓ Arterial blood pressure  ↑ Pulmonary artery pressure  ↓ CVP  ↓ Venous return  ↓ Cardiac output METABOLIC CHANGES  ↓ Total-body oxygen consumption  ↓ Total-body carbon dioxide production  ↑ Mixed venous oxygen saturation  ↓ Total-body oxygen extraction  ↑ Epinephrine and norepinephrine  Respiratory alkalosis  Metabolic acidosis METABOLIC CHANGES  ↑ Total-body oxygen consumption  ↑ Lactate  ↓ Mixed venous oxygen saturation  ↑ Prostaglandins  ↑ Activated complement  ↑ Myocardial depressant factor(s)  ↓ Temperature  Metabolic acidosis FACTORS INFLUENCING  Level of aortic cross-clamp  Species differences  Anesthetic agents and techniques  Use of vasodilator therapy  Use of diverting circulatory support  Degree of periaortic collateralization  Left ventricular function  Status of the coronary circulation  Volume status  Neuroendocrine activation  Duration of aortic cross-clamping  Body temperature  Duration & location of the aortic clamp determine the degree of hypotension observed  A supraceliac clamp can result in significant bowel & liver ischemia; decrease in SVR & CO after release of such a clamp can be significant THERAPEUTIC INTERVENTIONS  Anticipation of the increase in SVR is important  Heparinisation before clamp  Some vascular surgeons clamp the iliac arteries first to prevent distal embolization due to the aortic clamp AFTERLOAD REDUCTION  SNP  Inhaled anesthetics  Amrinone –PDE3#  Shunts and aorta-to-femoral bypass PRELOAD REDUCTION  NTG  Controlled phlebotomy  Atrial-to-femoral bypass OTHERS  Hypothermia  Soda Bicarb  Low minute ventilation THERAPEUTIC INTERVENTIONS  Anticipation of clamp removal is important.  Prior to clamp removal, increase preload. increasing the PCWP (if PAC used) by 3-4 mmHg above baseline  Discontinue agents such as NTG, nitroprusside & esmolol  Don‘t decrease anesthetic depth  Agents such as phenylephrine, ephedrine & epinephrine can be used  Raising BP 20-30% above baseline with such agents prior to clamp release is often necessary to avoid significant hypotension  Upon unclamping, acidic metabolites from the ischemic tissues below the clamp are washed back into the circulation  Prophylactic ventilatory adjustments to accommodate this increased acid load  Frequent ABGs
  • 50. 50  Renal protection strategies  buffer therapy with bicarbonate or THAM ( trisoaminomethane/tromethamine 0.3M)  After unclamping, reverse heparin  Discuss timing of reversal with surgeon.  ↓ Inhaled anesthetics  ↓ Vasodilators  ↑ Fluid administration  ↑ Vasoconstrictor drugs  Gradual release of clamp  Search for bleeding if ↓BP for more than 5min  Echo for cardiac function  Reapply cross-clamp for severe hypotension  Consider mannitol  Consider sodium bicarbonate Aortic cross clamp Passive recoil distal to clamp ↑catecholamines (& other vasoconstrictors) ↑ Impedance to aortic flow Active venoconstriction proximal & distal to clamp ↑ arterial resistance ↑ preload ↑coronary flow ↑contractility ↑Cardiac output↓ ↑ afterload If coronary flow & contractility increase If coronary flow & contractility do not increase
  • 51. Aortic cross clamping Distal tissue ischemia Mediators release Distal vasodilation ↑ venous capacitance ↓ arterial resistance ↑ permeability (by end of clamping period) Unclamping Mediators production & washout ↓ myocardial contractility ↑ pulmonary vascular resistance Pulmonary edema Loss of intravascular fluid Central hypovolemia Distal shift of blood volume ↓ venous return ↓ cardiac output Hypotension
  • 52. 52 Mature vs immature Ach receptor NICOTINIC ACETYLCHOLINE RECEPTORS: (2α,β,δ,ε,), (2α,β,δ,γ )& (α7) MATURE IMMATURE Also called Junctional conventional Extrajunctional Fetal γ-subunit receptor Structure 2α,β,δ,ε 2α,β,δ,γ After muscle fibre injury; within 18hrs Fetus before innervations Burns Trauma Motor neuron lesion: upper or lower Insulin resistance state Sepsis Prolonged immobility Not seen in muscle protein catabolism & wasting that occurs with malnutrition Half life Approx 2w <24hrs Channel feature shorter open times and high-amplitude channel currents during depolarization Long open times and low-amplitude channel currents. Fast-gated, high-conductance channel type Smaller single channel conductance & 2- 10fold longer channel open time Significance 1. Increased sensitivity to depolarizing agents 2. Decreased sensitivity to non- depolarizing agent 3. Stays open for a longer time: thus increased efflux of intracellular potassium: can lead to lethal hyperkalemi Note: all this channel are insensitive to treatment with muscarinic acetylcholine receptor antagonist, atropine, but sensitive to treatment with α-bungarotoxin or muscle relaxants, which block the flow of current
  • 53. Neuronal α7 AchR Muscular α7 AchR Choline do not open this Choline full agonist of muscle α7 AchR in conc. that do not open conventional AchR Readily desensitized. No desensitization occurs even in continued presence of choline allowing greater chance to efflux of K. Chemical α-conotoxin inhibits Does not get inhibited by α-conotoxin Methylcaconitine (selective antagonist of conventional α7 AchR) Muscular α7AchR also having low affinity for antagonist ( eg; pancuronium and α bungarotoxin), so high conc required. Conventional AchR antagonist bind with 1 α subunit whereas in these pentameric receptors 3 subunits are bind by an antagonist still 2 subunits available for binding to agonist and causing depolarization, resulting in resistance of α7AchR to blocking effect of drug. (eg: pancuronium)
  • 54. 54 Pattern of neuromuscular stimulation Feature ST TOF Tetanus DBS PTC Current strength Supramaximal Supra- or submaximal Supra- or submaximal Supra- or submaximal Supra- or submaximal Frequency 0.1–1 Hz 2 Hz four stimuli 30–50 Hz for 5 seconds Three impulses at 50 Hz repeated after 750 millisec 50 Hz for 5 seconds, 3 seconds later ST at 1 Hz Prerelaxant control Needed Not needed Not needed Not needed Not needed Pain on stimulation - -/+ ++ ++ ++ Sensitivity of manual detection (visual and tactile) Not sensitive Not sensitive at TOFR of 0.4 or more Sensitive Highly sensitive Sensitive Alteration of subsequent responses Not altered Not altered Altered (post- tetanic facilitation) Not altered Altered Interval between successive stimuli 5sec 12sec 2min 12-15sec 6min Receptor occupancy detection 75–90% 70–90% 70–90% 70–90% >90% Sensitivity for detection of subtle block Not sensitive Sensitive Sensitive Sensitive Not applicable Monitoring of profound block Not useful Not useful Not useful Not useful Useful
  • 55. TOF vs double burst TOF-TRAIN OF FOUR STIMULATION DOUBLE BURST STIMULATION Four supramaximal stimuli given every 0.5sec(2Hz) Two short burst of 50Hz titanic stimuli of 60ms duration and 750ms apart. The number of impulse in each burst can vary: in DBS3,3 : 3impulses in each of two burst, in DBS3,2: the first burst 3impulse, the second 2 impulse. Introduced in early 1970 1989 Most frequently used Less frequent Introduced to : make clinically reliable throughout all phases without need of any objective monitoring device To improve tactile or visual evaluation(clinical evaluation) of recovery from neuromuscular blockade Degree of block can be read directly even though preoperative value is lacking Do Information of onset, degree & recovery all obtained Do Simple nerve stimulator Require special stimulator Less painful more Differentiate depolarizing block & non-depolarizing do Useful for detection of block in the range of surgical relaxation(70-100% receptor occupancy) do Does not influence subsequent monitoring of degree Doses influence( as this involve titanic stimulation): may potentiate subsequent response Fade is accurate only when TOF ratio <0.4 i.e when TOF ratio b/w 0.4-0.9 fade cannot be detected either visually or tactile. So subjective method overestimate recovery.Thus need of objective measurement. Tactile fade is better appreciated at higher TOF. But still not well appreciated at TOF 0.6-0.9, thus this also cannot replace objective monitoring. No Fade indicates 70-75% receptors blocked 60-70% receptors blocked Does not quantify intense block(i.e at no response to TOF) do Does not monitor phase I block of depolarizing block do
  • 56. 56 BIS vs Entropy BIS ENTROPY Principle Statistical analysis of frequency domain (power spectrum, beta ratio) & time domain (burst suppression ratio) Amount of disorder in a system. Irregular EEG→↑entropy →awake. Regular EEG→↓entropy →sleep. Value range 0-100 State entropy(SE): 0-91 Response entropy(RE): 0-100 SE-RE=0-3 Cortical/subcortical activity Cortical Cortical & subcortical. If RE>SE (>10)→↑musculoskeletal activity (subcortical) SE: cortical RE: subcortical Electrode 1,2,4,3 1,2,3 Interference with electrocautery More Less
  • 57. Non depolarizing muscle relaxants: steroidal vs benzylisoquinolium vs Ether vs alkaloid NON-DEPOLARISING MUSCLE RELAXANTS STEROIDAL COMPOUNDS BENZYLISOQUINOLIUM COMPOUNDS PHENOLIC ETHER STRYCHNOS ALKALOID  Pancuronium  Pipecuronium  Vecuronium  Rocuronium  Ropacuronium(withdrawn bcoz of bronchoconstriction)  Gantacuronium(Shortest & fastest)  dTC(max histamine release)  Metocurine  Doxacurium(longest & most potent)  Cisatracurium  Atracurium  Mivacurium(shortest)  Gantacuronium(shortest & fastest under invest)  Gallamine(least potent)- nephrotoxic, teratogenic  Alcuronium high potency high potency long acting Long acting lack histamine release tendency to cause histamine release except doxacurium and cisatracurium - - vagolytic - strongly vagolytic Weak vagolytic hepatic Ester hydrolysis Hoffman elimination Not metabolized Not metabolized excreted by Kidneys Very less renal elimination, Only laudanosine (<30% excreted in kidney, 70% via bile) Excreted unchanged via kidneys Excreted unchanged in kidney Sugammadex can be used - - -
  • 58. 58 Scholine phase I vs phase II block COMPETITIVE BLOCK(D-TC) DEPOLARIZING (PHASE I) DEPOLARIZING (PHASE II) Paralysis in man Flaccid Fasciculations →flaccid Flaccid paralysis Paralysis in chick Flaccid Spastic Effect on isolated frogs rectus muscle No contraction, antagonism of ACh contractions Species sensitivity Rat > rabbit > cat Cat > rabbit > rat Human neonates More sensitive Relatively resistant Tetanic stimulation during partial block Poorly sustained contraction(fade) Well sustained contraction Unsustained(fade) Neostigmine Antagonises block No effect Antagonistic Post tetanic potentiation Present Absent Present Ether anaesthesia Synergistic No effect Order of paralysis Fingers, eyes → limbs → neck, face → trunk → respiratory Neck, limbs → face, jaw, eyes, pharynx → trunk → respiratory Effect of lowering temperature Reduces block Intensifies block Effect of cathodal current to end plate Lessens block Enhances block Structure-activity relationship: quaternary ammonium compounds similar to Ach Bulky rigid, do not activate muscarinic receptors More quaternary groups: longer acting, more potent Bridging structure between amines, lipohilic, determines potency Tertiary amine: histamine release Long thin flexible molecule: therefore has ganglionic, muscarinic effects End-plate membrane potential Depolarized to –55 mV Repolarization toward - 80 mV Onset Immediate Slow transition Dose-dependence Lower Usually higher or follows prolonged infusion Recovery Rapid More prolonged Mechanism Competitive blockade of Ach receptor Succinylcholine is comprised of two acetylcholine molecules joined together and acts as a depolarizing neuromuscular blocker by binding acetylcholine receptors at the post- synaptic neuromuscular junction end plate. The resultant end plate depolarization initially With increasing doses of succinylcholine (i.e., a large single dose, repeated doses, or a continuous infusion), a phase II block may occur. Continuous activation of acetylcholine receptors leads to ongoing shifts of sodium into the cell and potassium out of the cell.
  • 59. stimulates muscle contraction; however, because succinylcholine is not degraded by acetylcholinesterase, it remains in the neuromuscular junction to cause continuous end plate depolarization and subsequent muscle relaxation. This is termed a phase I block. Despite this, the post- junctional membrane potential eventually moves in the direction of normal even in the continued presence of succinylcholine. This is due to increased activity of the sodium-potassium ATPase pump, which brings potassium into the cell in exchange for sodium. The receptor does not respond appropriately to acetylcholine, and neuromuscular blockade is prolonged. Phase II block may be seen clinically with doses of succinylcholine >4mg/kg, but some characteristics of this blockade have been reported at 0.3mg/kg. Also called dual, mixed, or desensitizing block Seen in pseudocholinesterase deficient people
  • 60. 60
  • 61. Atracurium vs Cis-atracurium ATRACURONIUM CIS-ATRACURONIUM  Non-depolarizing neuromuscular blocking agent  Intermediate duration of action  Benzylisoquinolinium compound  Undergoes temperature and pH-dependent chemical(Hofmann) degradation.  Degrades to form laudanosine and a monoquaternary acrylate: do not possess neuromuscular blocking activity  Metabolites eliminated by Urinary and hepatic pathways  Cholinergic receptor antagonist  Recovery index: 10-15min  No dosage adjustment required when use in geriatric patients and patients with renal/liver impairment  Suitable for continuous infusion  Minimal chances of prolonged recovery A racemic mixture of 10 steroisomers, of which 14% is cisatracurium A cis-isomer of atracurium- Bisbenzyltetrahydroisoquinolinium‖ One of ten stereoisomers in atracurium besylate Different isomer groups of atracurium have different pharmacokinetics, the trans-trans group having the highest clearance and the cis-cis group the lowest uniform 39% Organ-independent Hofmann elimination (77%) Undergo ester hydrolysis also Does not appear to be degraded directly by ester hydrolysis. Onset: 3-4min Intermediate time of onset ≥ atracurium and rocuronium. Onset: 4-6min - 3 times more potent than atracurium Atracuronium Metabolism minor pathway HYDROLYSIS by nonspecific esterases in blood quaternary alcohol + quaternary acid major pathway HOFFMANN elimination Laudanosine + quaternary monoacrylate 82% protein bound
  • 62. 62 0.25mg/kg ED95 :0.05mg/kg during N2O/O2/opioid Anesthetic 0.12mg/kg ED50:0.026mg/kg Time to max block: 3.2min 5.2 t1/2β: 22-25 mins (30-45 mins for 2X ED95 dose 0.1mg/kg) 0.5mg/kg Recommended intubating dose: 0.15-0.2mg/kg Duration: 35-45min Duration:40-50min Elimination t1/2: 17-21min Elimination half-life 22-35 min CVS effect: tachy, hypotension due to histamine release absent Histamine release present( immune mediated or chemical mediated) No histamine release (up to and including 8 x ED95) when administered over 5 to 10 seconds. Significant Laudonosine 1/3 to 1/10 of that produced with Atracurium Benzyl alcohol present The 10-mL multiple-dose vials of Cisa are contraindicated for use in premature infants • benzyl alcohol; (oxidized to benzoic acid, conjugated with glycine in liver & excreted as hippuric acid)metabolic pathway not well developed: gasping baby syndrome 0.5mg/kg 0.1mg/kg 5mcg/kg/min 10mcg/kg/min • Initial dose: 0.15mg/kg or 0.2mg/kg • Maintenance: 0.03mg/kg generally required 40– 50 minutes after initial dose • Infusion dose: 1–2mcg/kg/min • under opioid/nitrous oxide/oxygen anesthesia • Infusion in ICU: 3mcg/kg/min Lung protective(anti inflammatory action) Plasma clearance: 6.1-10.9ml/kg/min 5.2 Volume of distribution: 18-280ml/kg 31( follow 2compartment model) Commercial preparation: 10mg/cc 2mg/cc It is acidic: not compatible with alkaline solutions>8.5pH
  • 63. Neostigmine versus sugammadex NEOSTIGMINE SUGAMMADEX CLASSIFICATION Anticholinesterase inhibitor Steroidal NDMR reversal agent CHEMISTRY 3-dimethylaminophenol derivative Cyclodextrin MOA By inhibiting anticholinesterase enzyme, it increases acetylcholine concentration at the synapse. Increased amount of acetycholine competitively reverse the action of NDMR. Envelops NMBA with high affinity binding & excreted in urine. Lipophilic inner core binds to Roc, Vec, Pan (in order of affinity). 1 molecule binds to 1molecule of NDMR. First neutralize NDMR present in plasma, then also dissociates NDMR at synapse. Duration of action Up to 4hrs Up to 24hrs Metabolism Slow hydrolysis by acetylcholinesterase & plasma esterases Not metabolized Elimination t1/2 50-90min 120min Vd 0.8lit/kg 11-14lit Clearance 1-16ml/min/kg 88ml/min Excretion 70% unchanged excreted in urine, 30% alcoholic metabolite excreted in urine Urine over 24hrs ADVANTAGES Cheap & easily available Rapid reversal(17times faster). When block is Shallow 2.2min(6.9min for neostig) Deep 2.7min (16.2min for neostig) Can be used for reversal of any type of NDMR Beneficial in obese ( in whom residual paralysis is hazardous eg. osa) Beneficial in elderly ( as they are prone for Postop pul comp) Other uses: myasthenia gravis, colonic pseudo-obstruction, snake bite, intrathecal additive for anesthesia, urine retention Rapid & predictable. So useful for airway rescue. Useful for any depth of blockade Makes rocuron useful in RSI, ECT and difficult airway(CICV) instead of suxamethonium Useful in myasthenia gravis for reversal , cardiac diseases to lessen side effects of neostigmine DISADVANTAGES Side effects: bradycardia, nausea, vomiting, abdominal crmps, diarrhoea, hypersalivation. Thus require co administration of anticholinergic (thus associated side effects too). Hypersensitivity & anaphylaxis: dose dependent Although can be sued for rocuron induced anaphylaxis Incidence is less compared to rocuron, neostigmine induced anaphylaxis. Dysgeusia, headache, fatigue, nausea, vomiting, dizziness Limited efficacy in reversing deep blockade Even though vecuronium can be reversed, it require twice the time of rocuron reversal (affinity for rocuron is 2.5times that of vecuron) Speed of recovery is unpredictable FDA approval for pediatric use is not available ( although it is safe, useful for airway rescue, similar dose as in adults) Ceiling effect when AChE inhibitors are Only useful for steroidal NDMR (note:
  • 64. 64 100% cysteine for novel isoquinoliniums, calabadion for all NDMR) Potentiate suxamethonium induced blockade Transiently increases aPTT & PT. (not significant at lower doses) Excess dose can itself lead to blockade like suxamethonium As exclusively excreted via kidneys, its safety not available in renal impairment patients. (Although sugammadex neutralize NDMR effect & not excretion of its complex in urine) Safety not available in pregnant women, breast feeding Patient using OCP will have contraception failure. So such patient should use backup methods like condoms. Co-administration with ondanset, verapamil & ranitidine lead to physical incompatability Cost & non availability Reversal when quantitative (objective) neuromuscular monitoring is available & reliable SUGAMMADEX no response to TOF PTC 0 16mg/kg PTC 1-15 4mg/kg TOF count 1-4 2mg/kg TOF<1 TOF<0.9 2mg/kg TOF> 0.9 NEOSTIGMINE TOF>0.9 TOF0.4- 0.9 0.02mg/kg TOF<0.4 or count 2-3 0.05mg/kg TOF 0-1 Delay reversal to TOF count of 2 No reversal