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36529437 Final Anesthesia Reviw Flash Cards Copy

36529437 Final Anesthesia Reviw Flash Cards Copy

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Published by: Fatos Katanolli on May 05, 2012
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King Fahad Medical City –Ryadh - Saudi Arabia

Page 1 of 217

He was kind enough to share them with his residents. They describe the important points-anesthetic concerns- in most common anesthesia topics, to help you prepare for the vaiva/case scenario exam.I hope that you will find them helpful in your exam as well as in your clinical works as it was for me.
A:airway. B:breathing/respiaratory system C:circulation/heart condition. D:drugs. M:metabolic concerns..lytes/glucose/ABG..etc. G:gastrointestinal system.

THA Page 2 of 217  Usually elderly Pt  If a revision   blood loss and it takes longer Epidural or GA  Look for the cause of arthritis  # due to CV disease (syncope) avascular necrosis due steroids, infarction (sickle cell disease)  Spinal Vs GA  less risk of PE with spinal and  blood loss A, B, C  look under elderly, and other co-existing diseases  Consider Autologus blood donation  Lab: ECG, CBC….. depend on the co-existing diseases  If suspect a difficult A/W  GA, due to position  Intra-op: risk of PE (cement, BM, fat) consider art-line in Pt with CV disease  Post-op: need to anticoagulated, pain epidural or PCA  DDx of circulatory collapse intra-op: PE, MI, total spinal, anaphylaxis

Thalassemia Page 3 of 217  Ethnic: Mediterranean, African-American, middle east and Asian  -thalassemia o major (homozygote) (Cooley’s anemia) severe, need treatment o intermediate (hetro) o minor (hetro) o manifest after 1st year of life, when Hb F disappears.  -thalassemia o 4 genes for the -chain synthesis o 1 gene deletion silent carrier. o 2 genes deletion mild microcytic anemia. o 3 genes deletion severe hemolytic anemia. o 4 genes deletion hydrps fetalis   GI absorption of iron and with multi-Tx  iron overload hemochromatosis .  treatment : o Tx and folate in mild form o Multi Tx and iron chelating agent in the severe form o Splenectomy

The Myotonias Page 4 of 217  delayed relaxation of skeletal muscle after voluntary contraction,  myotonic contracture is not relieved by regional, NDMR, or deep GA.  Relaxation may be induced by infiltration of the muscle with local anesthetic.  caused by genetic abnormalities that produce defects in sodium or chloride channels or proteins which alter ion channel function in muscle cells  giving drugs that Na influx into the cell and delay return of membrane excitability,like quinine, tocainide, or mexilitene, may relax myotonic contracture. Myotonic Dystrophy (Steinert's Disease)  is the most common form of the myotonias and the most severe.  AD inherited disorder (1 in 8000), S/S during the 2nd and 3rd decades of life.  clinical features associated with myotonic dystrophy: muscle degeneration, cataracts, premature balding, DM, thyroid dysfunction, adrenal insufficiency, gonadal atrophy, cardiac conduction abnormalities.  Cardiac abnormalities LV diastolic dysfunction, cardiac failure is rare. o AV block , A.fib, or flutter, ventricular dysrhythmias. o 1st -degree AV block may actually precede the onset of clinical symptoms o Sudden death may be a result of the abrupt onset of 3rd -degree AV block.

bronchial injury with blunt trauma Pt may have stridor. air leak. recurrent pneumo. loss of expiratory volume  Due to association with other injury. mainly c-spine  DLT is difficult to insert so consider other option  If chest tube drain >1L initially or >200ml/h  open  When putting a C-line  have it in the same side of the chest injury  Always be careful with PPV which can worse the hemodynamic with tamponade. and convert a pneumo to a tension pneumo  Complication of chest injury empyema. dyspnea S: subQ emphysema. wheezing.Thoracic trauma: Page 5 of 217  ACLS. persistence air leak. BPF . and in addition to other injuries  Heart and major vessels  Chest wall  flail chest > 3 ribs# need intubation with PEEP  Esophageal  Diaphragm  initially no S/S  then CXR diagnostic  Lung parenchyma  contusion  Tracheal. pneumomediastinum.

10% LAD from RCA  CXR:  pul vascular marking. RVH. RVOTO(sub. supra)  70% have bicuspid aortic valve. PCO2. defecation  Any thing that  PVR or  SVR  tet spells (PO2. crying. polycythemia  Pre-op: avoid dehydration. by age 6y  ferq & severity  Initiated by feeding. Rt aortic arch. ECG: RAD. overriding aorta. valvular. cyanosis. RVH  Tet spells: hypercyanotic attaches peak 2-6 m. and don’t upset them  Hemodynamic goals: o Preload  o R/R slow and sinus o cont  o SVR  o PVR  A N/A . acidosis)  Rt to Lt shunt  S/S: clubbing. F=M  VSD.TOF Page 6 of 217  Most common cyanotic CHD.

not  risk. may  PVR  Consider art-line . and no special precautions  May have a residual or recur VSD. or conduction abnormality after the repair  So for residual defect manage as TOF  hemodynamic Goals: o preload  o R/R  slightly  maintain sinus o Cont  maintain. avoid sudden  in SVR  No spinal  early epidural is desirable.TOF. or  pul outflow tract obstruction  All TOF need Echo for that reason  12-ECG  may have arrhythmias. obst Page 7 of 217  Corrected TOF. or slightly  o Afterload maintain.

bleeding  see other card o Pul edema  due to relief of the obstruction  frothy pink secretion in the ETT. Rt heart failure ECG. OSA. O2 . CXR. cor pulmonale. pain.  O2 sat. A/W obstruction wheezing . aspiration o Mx supportive  ETT. PPV with PEEP. abscess  A tonsils size(0-+4(75%)). chest retraction and  RR  C  CHD need Abx prophylaxis. Echo  D over counter meds may contain ASA  Induction  normal  Intra-op avoid NSAID’s . CHF.  RR o DDx  anaphylaxis . volume overload. ARDS.  sat. stridor  B OSA with snoring. dehydration.Tonsillectomy and Adenoidectomy Page 8 of 217  Peds considerations  Indication: recurrent tonsillitis. wheezing. diuretics o Usually subsided with in 24 hrs . give zofran and decadron  Post-op: o N&V.

with little and delayed  in HR  They are preload dependent  ECG may shows both donor and recipient P waves  No vagal input No bradycardia  But they response to stress(hypoxia. maintain preload D atropine and pancuronium No effect. in addition to the side effect of immunosuppressant drugs. PCO2) by  HR but it’s delayed  Premature CAD. with in 3 yrs. Norepi  -effect. CAD. glucose intolerance Heme anemia. and Abx coverage M adrenal suppression. and drugs.Transplanted heart Page 9 of 217  High risk of infection mainly cholecystitis  The efferent denervation is permanent. if they have Aff pain  The main symptom is dyspnea C altered response to stress. while some may retain afferent innervations  The response to exercise in normal heart is by  HR. thrombocytopenia . in a transplanted heart it’s by  SV. may need stress dose steroids. Neostgmine  may slow HR. mainly without angina. Adenosine  effect.

stabbing Burn  Same rule of nines apply to pregnant Pt  With inhalation injury CO poisoning  the fetus has a higher affinity to CO than the mother  Apply the same ATLS. and continue FHR monitor . maintain LUD  Have fetal US done.Trauma in pregnancy Page 10 of 217 Blunt  Closed head injury is the major cause of death  Other risks: o Uterine rupture o Placenta Abruption o Fetal injury o Spleen and liver rupture Penetrating  GSW.

and to lactate acidosis. CVP . hypoxia. nausea.  Volume overload  Lt heart failure pul edema  CNS S/S due to both the type of irrigation and the severity of  in serum Na  Management: o ABC. HTN. HR. and mental status changes. 100% O2. bradycardia. SOB. coma. and invasive monitoring art line. or dizziness) to severe (seizures. Anaphylactic reaction if CV collapse.TURP-TURB: Page 11 of 217  Distilled H2O hemolysis not used any more  Sorbitol converted to fructose hyperglycemia. intubate o Notify the surgeon to terminate the procedure o Consider DDx: over-sedation hypercarbia.  In the awake patient: a classic triad of symptoms  in both SBP and DBP associated with an  in pulse pressure. diabetic coma o 12 leads ECG. also well cause osmotic diuresis and dehydration  Glycine(inhibitory neurotransmitter) transit blindness ammonia  encephalopathy TURP Syndrome:( water intoxication syndrome)  S/S mild (restlessness. or CV collapse).

25g fulminant hepatic failure  Ingestion even a lower dose with alcohol   the chance of hepatic failure  Tylenol normally detoxified by conjugation to glutathione. RUQ pain with or without obtundation  After 24h symptom disappear and Pt looks well  24-72h  liver failure appear. then 50mg/kg over 4h then 100mg/kg over 16h o Look at the nomogram . but with overdose  glutathione depleted metabolized by P-450 to a toxic compound  First few hr after N&V. encephalopathy and acidosis   bilirubin correlate with  survival  Management: o ABC o Mucomyst.Tylenol overdose Page 12 of 217  A single dose of 10-15g can produce liver injury. with best result if given 12-20h after ingestion o Roughly 150mg/kg over 15min. coaglupathy. with possible ATN. and cardiotoxicity  Poor prognosis with  Phos.

adrenal insufficiency G  obstruction.Ulcerative Colitis A may have Ankylosing spondylitis  difficult A/W. metabolic acidosis. perforation Page 13 of 217 .  albumin. with S/S bowel obstruction  RSI B  possible restrictive lung disease with ank-spond C AR. hypovolemia D steroids (stress dose) M  electrolytes imbalance. K .

Upper Ext nerve injury: Page 14 of 217 Ulnar:   sensation over the 4th and 5th fingers  Muscle wasting. with weakness of arm abduction . loss of sensation over the lateral aspect of the forearm Axillary N  Loss of skin sensation over the lower ½ of the deltoid muscle. also loss of thumb flexion Radial:  If the injury at the axilla  unable to extend the forearm (triceps)  If in the spiral groove  wrist drop MCN:  Loss of arm flexion (biceps). when making a fist  the index and middle finger remain straight. unable to grip a paper between fingers Median:  Loss of skin sensation over the lateral 3 ½ of the palm of the hand  Weakness of wrist flexion.

So 2-4 wks is reasonable . the child may end up with another episode of URTI. >1 yr   temp  postponed  Elective > 1yr  normal temp  P/E  purulent secretion.URTI Page 15 of 217  Need to distinguish from allergic rhinitis   incidence of croup. and < 1yr  postponed  If elective. and laryngospasm  If emergency or urgent surgery proceed. bronchospasm. LRTI  postponed  = = = =  clear  proceed to surgery  How long to postponed for. if too long. and anticipate the above problems  If elective.

hypotension Heme bleeding. anemia Mx  See abruption card  Basically same management they come for stat C/S due fetal distress Page 16 of 217 .Uterine Rupture  Risk see box 37-1 chestnut  Mainly fetal distress and bleeding A & B  onst C hypovolemic shock.

and PEEP which may cause paradoxical embolism .VAE: Page 17 of 217  When the surgical field > 5cm above the Rt atrium.  40-50% in the sitting position. By TEE the most sensitive then pericardial doppler. avoid sitting position  Dx. placed in the Rt sternal border 3rd to 6th intercostal space. if known PFO. which detect 0. flood the surgical field with saline gauze Wax the bone edges Compress the jugular vein Head down Aspirate through the CVP D/C N2O.25ml of air  Miller all Pt going for N.surgery in sitting position need to have CVP  Mx: 100% O2 Notify the surgeon.

recombinant Vwf. N PT and PTT  I (70-80%) vWF.  Hematology consult.3ug/kg 1hr prior to surgery. group O blood have 20-30% less vWF  Prolonged bleeding time. III(very rare). Possible HIV +  Do gentle intubation.von Willebrand's Disease Page 18 of 217  AD.  DDAVP may cause fibrinolysis by releasing t-PA so consider giving TXA  Cryo have vWF . 3types I. avoid blind suctioning. IIA also function abnormal. avoid Regional anesthesia . II.  Pregnancy  vWF  Rx  DDAVP 0. IIB they have thrombocytopenia which aggravated by giving DDAVP (C/I).

the larger. with normal ECG and CXR  mod also asymptomatic. with biventricular enlargement on CXR  large when pul blood flow > systemic. low forward CO . and the lower PVR  more severe symptom  small asymptomatic. with S/S depend on the size. S/S early as 4 wks.VSD Page 19 of 217  Rare in adult . load pansystolic murmur Lt sternal border. CHF. Lt Rt change to Rt Lt  cyanosis  hemodynamic goals: o Preload  o R/R N and sinus o Cont slight  o Afterload  o PVR  Pre-op Abx prophylaxis A N/A B pul edema C shunt. and PVR.

cryoprecipitate. and patients immunocompromised by many other disease processes. It has not occurred following transfusion of FFP. nausea. headache. granulocytes. platelets. plasma.  Febrile reactions can be treated with acetaminophen  should be distinguished from a hemolytic transfusion reaction (direct Coombs test) Graft-versus-Host Disease (GVHD)  the donor lymphocytes may become engrafted. and a nonproductive cough. and establish an immune response against the recipient. packed RBCs. myalgias. not frozen. and the fatality rate is very high  Also when a genetic relationship exists between the donor and the recipient  GVHD has been reported with the transfusion of whole blood.  the patient experiences a temp  of more than 1°C within 4 hrs of a blood Tx and defervesces within 48 hours. GVHD typically progresses rapidly to pancytopenia.White Cell–Related Transfusion Reactions Page 20 of 217 Febrile Reactions:  antibodies to the HLAs after multiple Tx. 1% of all RBC transfusions. or frozen RBCs . anxiety. neonates who have undergone a blood-exchange Tx.may also develop chills. proliferate.  Patients at risk for GVHD include organ transplant recipients. respiratory distress. and fresh.

emptying  RSI B lung mets. m a z e n . chemo. Lytes CBC other upper body IV access Potential intra-op problem IVC obstruction  CO Tumor in the IVC  embolic phenomena Post-op  ICU backup mazen h o m e o f f i c e . severe if both kidneys involved  CHF. acquired vWD possible need F VIII concentrate M art. and radiotherapy effect C HTN.Wilms tumor Page 21 of 217 A delayed G.  renin secretion D chemo R hyperaldosternism(2nd) K H severe anemia.and central line Lab X-match. low PLT.

IV worming device. with blood set  Lines: Big 14G peripheral IV. PFT. Mg. Lytes. Echo if available  Consider optimizing any medical condition pre-op by meds. and high risk of blood loss A N/A B potential COPD C CAD. Art line. TEE  Induction: routine. creat. bear hugger  Monitors: standard + 5 leads ECG.  X-match for at least 6 U of blood.AAA Elective Page 22 of 217  Long procedure. CVP/PAC. consultation. ECG. HTN. Foley. art-line. and further evaluation. Renal border line function  In the pre-op evaluation: concentrate on cardiac function with detailed H/P and work up  Lab: CBC-D. large fluid shift. CVP/PAC. modify on cardiac status  Before induction have inotrops and vasodilators ready to go . ABG. CXR. temp. have FFP ready  Consider Epidural to do it as a combined technique  Have the cell saver in the room. BUN.

BUN. Mx:  Depend on the severity. may end up need hysterectomy . and can have 2500ml of blood  DDx placenta previa. fibrinogen. RSI. creat. LUD  Lab CBC. induction with Ketamine.  age  Most common cause of DIC. and DIC Fetus  Demise. smoking. PTT. Lytes. trauma. hemoabt(PGF2). usually partial managed conservative with bed rest  ABC. Heme anemia. fetal monitoring . GI prophylaxis. hypoxia. large IV  Synto may not work  atony consider ergot. PT. risk ante-postpartum hemorrhage. uterine rupture A obst B obst C hypovolemic shock. X-match  Monitor  Art line. D-dimer . coaglupathy  DIC R ARF from both shock.Abruptio placenta Page 23 of 217  Risk  with cocaine abuse. previous abruption. CVP/PAC. fetal hypoxia  The bleeding could be concealed.

Echo. possible  ICP. pul HTN CNS hydrocephalus.Achondroplasia: A potential difficult A/W. MRI base of the skull. ECG. central sleep apnea  Lab CXR. C-spine. OSA B Kyphoscoliosis  Restrictive lung disease C Cor-pulmonale. CT. foramen Magnum Stenosis Avoid neck extension . PFT. in addition to the regular blood work Page 24 of 217 .

Position  nerve compression Monitors  art line . CHF. epiglottis. CXR. Echo) D  steroids for other pituitary problems N  neuropathy (document). Cardiomegaly. adenoma effect ? pressure  vision M DM. and potential post-op A/W obstruction B OSA C HTN. arrhythmias. hemodynamic instability (ECG.Acromegaly Page 25 of 217  99% from pituitary adenoma A large tongue . cardiomyopathy. hyperthyroid. possible vocal cord paralysis. and subglottic stenosis  smaller ETT. large nose  difficult intubation and mask fitting Need FOI.

pregnancy. and long bone #  The main effect is on the CVS: o Initial PSN effect with hypotension and bradycardia. arrhythmias and  ICP and IOP  Review the old anesthetic record for the dose. SOL with  ICP. and any problems may had happened  Also review all Pt med (TCA. possible difficult to obtain an accurate medical history  C/I: Pheo. MAOI)  avoid indirect sympathomimetics. also be careful when direct acting drugs  exaggerated response  Monitors  standard CAS monitors. know what is the program . consider invasive monitoring in sick Pt  Pt with pacemaker or AICD not C/I have the magnet in the room. recent CVA and MI. even arrest o Followed by intense SNS activation with HTN. tachycardia.ACT Page 26 of 217  Mainly for depression.

hyperventilation. and hypotension both  hepatic blood flow . exposure to toxins at work A  LOC B hypoxia. V/Q mismatch D altered drug metabolism M lytes abnormalities Renal impairment CNS  encephalopathy Heme coags abnormalities  Avoid sedation pre-op  Correct coags pre-op  Intra-op avoid hypoxemia. drugs.Acute liver dysfunction Page 27 of 217   M&M  Postponed if not an emergency  History of alcohol.

Acute pericarditis. with sinus tachy. if suspected effusion or tamponade  Normal pericardial fluid 20-30 ml. chest exam  friction rub. o In chronic effusion the pericardium can accommodate up to 1000 ml. with diffuse ST-elevation in ECG pericardial leads.  Consider Echo. without S/S of tamponade o But in acute effusion as low as 200 ml can give symptoms . and effusion Page 28 of 217  Most common cause is viral infection  Post-MI  Dressler Syndrome  S/S diffuse chest pain.

metastatic cancer. BP. muscle weakness. causes both a gluco and a mineralocorticoid deficiency.Adrenal Insufficiency (Addison disease): Page 29 of 217  Need 90% destruction of the adrenal gland to produce symptoms  primary (Addison's disease) is idiopathic adrenal insufficiency due to autoimmune destruction. surgical ablation. hyperpigmenation in primary only  Dx by ACTH stim test . from tumor. N&V.  Other: bacterial or fungal infections. aldosterone is maintained  S/S Wt loss. sepsis and hemorrhage.  Secondary: anterior pituitary fails to secrete sufficient quantities of ACTH.( less severe S/S.  Hashimoto's thyroiditis in association with autoimmune adrenal insufficiency is termed Schmidt's syndrome. abd/back pain due bleeding. or radiation therapy. infection.

or shock  Have inotrops support ready. and the complication of the repair. cardioversion. use saline instead of air for epidurals. Sequelae.  When.  In case of shunt  be meticulous about air in the IV.  In case of pulmonary HTN have NO in the room . What. recent Echo.Adult with repaired CHD Page 30 of 217  Type of CHD. (Repair)  Understand the physiology of the repair  Residue.  Follow up with cardiologist. if not ask for one  Discuss the case with a college who knows more about CHD(peds cardiac anesthetist)  The Need for SBE prophylaxis  High risk for arrhythmia (pads on) for pacing. and Where.

avoid cardiodepressant o Afterlaod   Epidural is good Page 31 of 217 . LUD o R/R  slightly  maintain sinus o Cont  maintain.AI  Well tolerated in pregnancy  hemodynamic Goals: o preload maintain.

Avoid PPV. depend on the Severity of the symptoms and hypoxemia may consider CXR( most are radiolucent).Airway foreign body Page 32 of 217  Emergency and potential life threatening  In addition to peds consideration  Brief H/P AMPLE. and racemic Epi . but may see atelectasis  Do inhalation induction with Sevo. minimal support if needed  Assess the eye for depth (see later)  The dilemma  Full stomach Vs need of maintaining spontaneous Ventilation  Once the eye in stage III  do direct laryngoscopy  Lidocaine spray  May give IV bolus of propofol upon the removal of the foreign body  Consider a dose of decadron .

stenosis. and risk of air embolism The metal-ETT are bigger than the PVC tubes so use one size smaller . other Jet ventilation Pt need to be completely paralyzed In case of airway fire remove ETT. reintubate with new ETT. CT The airway is shared with the surgeon close communication Eyeglasses and laser mask. and metal shields. keep intubated. have 60 cc syringe filled with NS ready. flow volume loop. avoid high Fi02 initially till you make sure that there is no ongoing fire direct laryngoscope. and fill the cuff with NS with methylene blue Avoid N2O.Airway laser surgery:          Page 33 of 217    Risk for both the patient and OR personal Knew what is the indication papiloma. cover the exposed skin with wet towels Consider glyco pre-med Use laser-metal ETT. bronchoscope with possible lavage and CXR. Pt eyes closed. Abx. covered with wet gauzes. after controlling the fire asses the airway damage.01 mm penetration less bleeding and edema post-op With Nd-YAG laser deeper penetration. neoplasm  PFT. use the lowest FiO2 possible < 40%. and steroids ICU post-op CO2 laser only 0. and ongoing fire.

is determined as follows: .Equations alveolar gas equation: Page 34 of 217 Shunt equation ventilation–perfusion ratio (VQI).

100% O2. hemorrhage R ARF CNS seizure Mx:  ABC. pul edema C cardiopul collapse. Lab as abruption. RV failure D  D/C synto Heme  DIC.LUD. obst B hypoxia. Large IV. last thing to do CPB (case report)  If Pt survive  ICU .Amniotic fluid embolism Page 35 of 217  Catastrophic event with high mortality rate 86% A  LOC.

Amphetamines  For management same as cocaine A&B obst C HTN arrhythmias. with possible arrest Ecstasy:   serotonin and dopamine level C HTN arrhythmia H DIC. tachycardia D  MAC with acute intoxication. MSK rhabdomyolysis M+R lytes abnormality. while chronic  MAC CNS seizure Obst  risk of abruption  R. anesthesia  severe hypotension. ARF Fetus toxicity Mx Page 36 of 217 .

ECHO. CXR. ABG. restrictive myopathy.Amyloidosis: Page 37 of 217  Extracellular deposition of amyloid type protein A macrogolssia. Art-line. nephritic syndrome Heme Factor X deficiency  Lab/DI: CBC. coags  Monitoring: CAS. BUN. CVP/PAC. CHF. Creat. avoid any nephro-toxic drugs  Have an ICU backup . autonomic dysfunction Renal CRF. tracheal stenosis (smaller ETT) B pul edema from CHF C arrhythmias. PFT/ flow volume loop. TEE  Avoid Regional if coagulopathic  The main goal intra-op is to maintain U/O. ECG. lytes.

with thyroid dysfunction  Do Regional technique better  If GA: Mod RSI. ICU post-op . M abnormal glucose and Ca metabolism.  sensitivity to NDMR. fasciculation and muscle atrophy A bulbar involvement  Aspiration  mod RSI B respiratory failure C D Sux C/I.Amyotrophic Lateral Sclerosis (ALS) Page 38 of 217  Degenerative disease of the CNS with involvement of both UMN and LMN  S/S Asymmetric weakness.  reflex.

Electrolyte abnormality Myocardial contusion. Fluid overload Hypothalamic infarction. Hypothermia Hypoxia. hemorrhage) Neurogenic shock Hypoxemia Neurogenic pul edema.Anesthesia for organ donation: Page 39 of 217 COMMON PHYSIOLOGIC DERANGEMENTS AFTER BRAIN DEATH Condition Cause Hypotension Hypovolemia (DI. for  BP consider use vasodilators . Pul contusion. Exposure Hypothermia Dysrhythmia (especially bradycardia)      Intracranial injury or herniation. Pneumonia Gastric aspiration. ischemia Avoid vasopressors  may cause visceral ischemia Consider using low dose Dopamine if needed They are atropine resistance Consider use NDMR due to somatic spinal reflex No need for GA.

 heat production with more prone to hypothermia GI/hep  gastric empting. Na losing . stiff ligament  difficult epidural/spinal heme anemia  Always IV wormer.  response to hypoxia and hypercarbia C diastolic dysfunction.Anesthesia For The Geriatric Patient Page 40 of 217   physiological reserve of all organs  Common diseases with aging are Sleep apnea. arrhythmias. arrhythmias. HTN.  hepatic mass and blood flow Renal   GFR. CHF D  Vd.  drugs clearance.  MAC. with  both hepatic and renal clearance. dementia. Alzheimer A  stiff neck B CC. bear hugger. DM. CV. CAD.  Na. risk of volume overload CNS Alzheimer. CAD. HTN. arthritis. COPD. V/Q mismatch.  sensitivity to narcotics and sedatives M DM. and consider invasive monitoring .

Aneurysm Page 41 of 217  F>M. unless they do temporary clipping . BUN. N&V. ECG. U  role out IHD M lytes disturbance. Creat. SIADH. usually present with SAH  Aneurismal SAH classification by Hunt & Hess and WFNS to estimate the surgical risk and outcome  WFNS Grade GCS Scale* Motor Deficit  I 15 Absent  II 13–14 Absent  III 13–14 Present  IV 7–12 Present or absent  V 3–6 Present or absent A LOC B pul edema C HTN. X-match  Induction as Supratentorial  May need controlled hypotension. Lytes. ECG changes ST. LOC  Lab: CBC. photophobia. pituitary dysfunction  Classic S/S: headache. review CT/MRI. DI. QT. T. CXR.

difficult to perform neuraxial block by midline approach. 20-30 y. CHF due to cardiomyopathy. possible difficult intubation . HLA-B27 is +ve in 90% of Pts  S/S: back pain and stiffness improve with exercise. Spines: limitation in the movement of all the spines. consider PFT C: Aortitis with AI. ? C/I if pt have peripheral neuropathy.  chest wall compliance and  VC. Renal  risk of RF Drugs: anti-inflammatory drugs Better to extubate awake Intervertebral ligament calcification. TMJ involvement. lumber disc degeneration.Ankylosing spondylitis Page 42 of 217  M>F. . with  risk of C5-C7 #. Cricoarytenoid involvement (rare) B: restrictive lung disease. dysrhythmias secondary to cardiac conduction system involvement.o. -ve rheumatoid factor. sacroilitis A.

Aortic Regurgitation Page 43 of 217  Chronic: rheumatic disease. nonpenetrating trauma. with pul congestion. connective tissue diseases including Reiter's syndrome and ankylosing spondylitis. and eventually symptoms of right-sided CHF with ascites and peripheral edema. or head pounding. ascending aortic aneurysm dissection Pathogenesis  Chronic: LV volume overload LV dilationLVH eccentric hypertrophy  LVEDV but LVEDP still normal over time  LVEDP  Acute: severe AR LV volume overload. with later development of orthopnea and PND. including fever with infective endocarditis.  Acute severe AR Patients typically exhibit symptoms referable to the underlying disease. . which may be nocturnal. hypertensive and atherosclerotic diseases. and chest or back pain with aortic dissection.  Acute: infective endocarditis. History: chronic AR usually remain asymptomatic for years. Exertional dyspnea may be the first manifestation of LV decompensation. cystic medial necrosis with or without other features of Marfan's syndrome.  Symptoms of more advanced disease include angina pectoris. luetic (syphilitic) aortitis. palpitations. but without time for LV dilation. mortality rate is estimated to be more than 10% per year among patients with severe AR and angina pectoris and more than 20% per year among patients with symptoms of CHF.  Prognosis worsens with the onset of symptoms.HR is the only comp mechanism to maintain forward CO. Early symptoms include a sensation pounding in the chest. LVEDP and LAP  rapidly.

or senile degenerative (calcific) in origin.5-3.  therapeutic decisions typically are based on the presence of symptoms in the setting of significant aortic stenosis. so patients may have low gradients despite severe AS if there is LV systolic dysfunction. categorization of disease as mild. ridge or tunnel stenosis. and syncope.0 cm2.0 to 1. severe <1.  Angina occurs without CAD resulting from  O2 demand from  LV mass and  intracavitary pressures in the setting of a fixed blood supply and from  coronary flow due to progressive outflow obstruction.0 cm2. angina pectoris. (life expectancy < 5 yrs)  Dyspnea due to in LVDP. mild 1. AS is not usually of hemodynamic significance until the valve area is  to 25% of normal. and pulmonary venous pressures.5 to 3. LA. and dynamic subvalvular LV outflow obstruction in HOCM  The normal AVA is 2. moderate 1. with  in peripheral oxygen requirement in the setting of a fixed CO. With normal CO. rheumatic. severe AS mean transvalvular pressure gradient 50 mm Hg. moderate.  Transvalvular gradients are affected by flow. including congenital supravalvular stenosis and subvalvular membrane.  Syncope may be caused by peripheral vasodilation with exertion.5 cm2. History long latent period >30 yrs  The three classic symptoms associated with aortic stenosis are dyspnea. or severe is of lesser clinical importance. Etiology congenital (bicuspid).Aortic Stenosis Page 44 of 217  Valvular AS should be distinguished from nonvalvular forms of LV outflow obstruction. .5 cm2.

epidural . with possible bowel obstruction  Usually in elderly with other co morbidities  With bowel prep  fluid deficit  hypotension upon induction A RSI (b. elderly Position lithotomy. with  intravascular volume GI Vomiting. jackknife Monitors CAS.Appendectomy  In older Pt consider other and possible catastrophic problem (AAA) A full stomach (RSI) C dehydration. Creat. art line. full stomach M Lytes abnormalities. temp. obstruction) C hypovolemia. acid base disturbance Other could be septic Lab CBC-D. lytes. BUN. foley Pain PCA. ABG Pain PCA Page 45 of 217 APR  For rectal Ca.

may put a donut where the defect is in the hall. due to hydrocephalus  awake intubation B vocal cords paralysis trach. resp depression due to post fossa compression C bradycardia CNS  the defects. and CN palsy  position as above  .Arnold chiari malformation Page 46 of 217  It’s one of the chiari malformation it’s type II  associated with myelomeningocele  present for posterior fossa decompression and repair of myelomeningocele and insertion of shunt  on of the main issue is position during induction due to myelomeningocele. if big may have to the induction in lateral position then turn prone A potential difficult airway.

avoid cardiodepressant o Afterlaod . to maintain PCWP =18  GA opioids. CVP/PAC risk of arrhythmia with insertion.AS Page 47 of 217  Mild  well tolerated  Mod/severe not well tolerated  hemodynamic Goals: o preload maintain. avoid sudden  in SVR  Need are-line. treat hypovolemia aggressively o R/R  slightly  maintain sinus  treat arrhythmia aggressively o Cont  maintain. LUD. pads on the Pt ASD:  3 types: ostium secundum @ foramen ovale . mix kitamine/STP  Have the crash cart in the room.

and optimize pre-op  If Pt is steroids (PO) dependent asthma consider steroids coverage peri-op  Pre-med -agonist. if yes when was the last one. how he/she manage the asthma at home.  Emergence: consider extubate deep. Exam: V/S. may consider LMA  Maintenance: avoid any histamine releasing drugs. IV Lidocaine pre-extubation  Consider regional anesthesia to avoid intubation . wheezing  Review PFT results pre-post bronchodilators. avoid STP. A/E .  Induction: IV Lidocaine. Anticholenergics. or need ER visit.Asthma: Page 48 of 217  H/P: how bad is the asthma? Severity? Frequency? Any hospital or ICU admission in the past. intubate deep.

pul edema. seizure. stimulator  show resistance N deficit  Neuraxial  best is a good choice but may be difficult to assess the level of the block too high.  post-op vent (ICU) C hyperreflexia. D (Sux C/I). 2-3 weeks after injury  Stimulation below the level of transection Severe HTN with bradycardia A potential difficult A/W. ABG. (RSI) B  respiratory reserve and volumes. orthostatic hypotension.  Sequelae  CV collapse. arrhythmias. unstable C-spine. ECG. pneumonia.Autonomic hyperreflexia: Page 49 of 217  Post spinal cord injury above T-7  70-75%. death . or too low  Hyper-reflexia may happen post-op due to bladder or rectal distension. have anti-HTN ready (Niprid) N. PE. stroke. assess the volume status. following the resolution of spinal shock. respiratory failure  PFT. risk of aspiration. aspiration risk (FOI).

 ICP  Pt may have (NPPB) normal perfusion pressure breakthrough  cerebral hyperperfusion with normal CPP o Rx: diuretics.AVM: Page 50 of 217  M>F. Sz.  LOC. N-low MAP. hypervent. high dose STP  The rest of management like Aneurysm  High risk of bleeding  blood in the room . SAH. motor/sens deficit  In Peds  Vein of Galen AVM  hydrocephalus + high output cardiac failure A  LOC B aspiration during Sz C CHF CNS Sz. 10-40yrs  S/S parenchymal hemorrhage. mild hypothermia.

Airway laser surgery: Page 51 of 217  Risk for both the patient and OR personal  Knew what is the indication papiloma. flow volume loop. and metal shields  Consider glyco pre-med  Use laser-metal ETT. bronchoscope with possible lavage and CXR. reintubate with new ETT consider ICU post-op . and fill the cuff with NS with methylene blue  Avoid N2O. other Jet ventilation  Pt need to be completely paralyzed  In case of airway fire remove ETT. use the lowest FiO2 possible. CT  The airway is shared with the surgeon close communication  Eyeglasses. after controlling the fire asses the airway damage direct laryngoscope. have 60 cc syringe filled with NS ready. Pt eyes closed. stenosis. covered with wet gauzes. neoplasm  PFT.

awake adult with eyes closed.g.. deep anesthesia. light anesthesia . hypoxia. brain tumors.EEG FREQUENCY RANGES Page 52 of 217 Delta rhythm (0–3 Hz) Deep sleep. predominantly seen in occipital leads Beta rhythm (>13 Hz) Mental activity. or pathologic states (e. hyperventilation in awake children and young adults Alpha rhythm (8–13 Hz) Resting. metabolic encephalopathy) Theta rhythm (4–7 Hz) Sleep and anesthesia in adults.

cramps. LOC. liver disease. so it’s result from excess or deficit of water  total body Na regulated by aldosterone and ANP. risk factors (alcoholism. areas of demyelination are apparent on MRI. not more than 25 mEq/l/48 hrs  Rapid correction  abrupt brain dehydration central pontine myelinolysis mild (transient behavioral disturbances or seizures) to severe (including pseudobulbar palsy and quadriparesis). use the following equation: Current [Na+] × current TBW = desired [Na+] × desired TBW TBW= 0. and hypokalemia) . weakness. tumor.6x wt .Within 3 to 4 weeks of the clinical onset of the syndrome. mediated by BNP. independent of SIADH. and infection  SIADH  see other card  Rx < 120 with 3% NS @ 1-2 ml/kg/hr to  serum Na 1-2 mEq/l/hr only for few hrs. coma and seizure  Acute CNS S/S is due to cerebral edema  What is the serum osmolality see figure  Cerebral salt wasting syndrome. cerebral hemorrhage and CHF  Once serum Na > 120 fluid restriction is enough . SAH.Hyponatremia < 130 Page 53 of 217   or  in serum Na   &  in ECV & PV. Also treat the underlying causes To calculate the net water loss necessary to  [Na+] in hyponatremia. where serum [Na] by ADH  S/S depend on the rate and severity of  of Na: loss of apatite. burns. risk head trauma. N&V. poor nutritional status.

infected cyst) b. Upper lobectomy 2.INDICATIONS FOR ONE-LUNG VENTILATION ABSOLUTE 1. Pneumonectomy c. Major bronchial disruption or trauma 3. Unilateral lung lavage 4. Unilateral cyst or bullae d. Video-assisted thoracoscopic surgery RELATIVE 1. Isolation of each lung to prevent contamination of a healthy lung a. Bronchopleural cutaneous fistula c. Infection (abscess. Middle and lower lobectomy c. Thoracic aortic aneurysm b. Surgical exposure—low priority a. Control of distribution of ventilation to only one lung a. Thoracoscopy under general anesthesia Page 54 of 217 . Bronchopleural fistula b. Esophageal surgery b. Massive hemorrhage 2. Surgical exposure—high priority a.

a large tongue. and an omphalocele. Induction: NG  aspirate gastric content then RSI . and arterial line Post-op keep intubated .Omphalocele and Gastroschisis Page 55 of 217 o Impaired blood supply to the herniated organs. need large IV . hypoglycemia. B respiratory failure C CHD in 20% of infants with omphalocele. possible central. congenital heart disease. and intestinal obstruction o Major intravascular fluid shift and dehydration full-strength balanced salt solution o Hypothermia and hypoglycemia A possible difficult airway  Beckwith-Wiedemann syndrome consists of mental retardation.

Stroke & TIA: Page 56 of 217  Hemorrhagic or ischemic  Etiology: Atherosclerosis. arrhythmias  ECG. and hyperglycemia  With chronic HTN the cerebral autoregulation curve shifted to the Rt . trauma. CAD. A. embolic  MI. A. ASA. Echo D anti-PLT. coumadin N   LOC Peri-op  Avoid swinging in BP.fib. VHD. loss of A/W reflux (RSI) B hypoventilation C HTN. post-op  CEA. severe HTN A  LOC.fib. VHD.

Bioterrorism Page 57 of 217  Use of nerve gases which are a potent Ach.esterase inhibitor and cause a cholinergic crisis  A mass casualty with both physical trauma and gas intoxication  Healthy soldiers Vs civilian with different age groups and other comorbidities  The amount. and protect the health care personal . also carry more risk to the health care personal with direct contact  All the nerve gases causes irreversible inhibition to AchE in both central and peripheral NS  The key point in the management is to give the antidote ASAP. and gradual S/S local muscle twitches and fasciculation (nicotinic effect) then resp failure. wheezing. duration and the rout of exposure are the major determine of the clinical course of intoxication  Exposure to vapor gives respiratory symptoms (SOB. bronchorrhea) with rapid cardiopulmonary collapse (muscarinic effect)  Where dermal exposure slow.

COPD. tumor  Most of the Pt with major co-morbidities e. Sepsis. gangrene. but be aware of risk thrombus embolization PE  Post-op pain(epidural. infection. DM. PVD.g. CAD.  H/P standard + depend on the co-morbidities  Lab also as above  Options: GA Vs spinal/epidural may  the incidence of phantom limb pain. nerve block. MI. DVT (S/C heparin). PCA). CVA. bleeding . DM.BKA Page 58 of 217  For PVD. CVA. CRF. trauma. but look for C/I  monitors standard + depend on the above co-morbidities  Position  risk of ischemic necrosis (pads)  EBL 250 ml  The use of tourniquet  bleeding.

traumatic rupture of a bronchus or bulla ( barotrauma or PEEP).BPF and Empyema Page 59 of 217  Causes: after pulmonary resection for carcinoma. and avoid N2O  For non-surgical management: DLT and resting the affected lung. loss of air with  alveolar ventilation and CO2 retention. penetrating chest wound. and potential tension Pneumothorax  In case of empyema with BPF drain the empyema under LA with chest tube under suction. then do a CXR. or use of HFJV  Keep a high index of suspicion for tension Pneumothorax . then may fix the BPF under GA  GA options ( the main target is to avoid PPV) o Awake intubation with DLT o Gas induction and maintaining spontaneous ventilation o RSI  Keep FiO2 always 1. or spontaneous drainage into the bronchial tree of an empyema cavity or lung cyst  PPV contamination of the healthy lung.

Brain death Page 60 of 217 ―irreversible cessation of all function of the entire brain. determined in accordance with accepted medical standards‖ CRITERIA FOR THE DIAGNOSIS OF BRAIN DEATH:  LOSS OF CEREBRAL CORTICAL FUNCTION o No spontaneous movement o Unresponsive to external stimuli  LOSS OF BRAIN STEM FUNCTION o Absent respiratory reflex (apnea test) o Absent cranial nerve reflexes (Gag or cough reflex to suction) o Pupillary light reflex ( no pupil constriction) o Corneal reflex ( no blinking with corneal touch) o Oculocephalic reflex ( doll’s eyes) o Oculovestibular reflex (cold caloric test) o Atropine resistance  SUPPORTING STUDIES o Electroencephalography . including the cortex and brain stem.

rate of production and absorption 0. volume 100-150 ml. Iso 0/  resistance  ICP N= 10 mmHg.5 ml O2  the autoregulation is abolished by trauma and hypoxia  CSF from the choroids plexus and absorbed by the arachnoid villi.4 ml/min.5 ml/100g/min& 5. and no change in CMRO2  All IV drugs cause  CBF and  CMRO2 .Brain metabolism and physiology: Page 61 of 217  In adult:O2 3.3-0.5 mg/100g/min of glucose. except N2O  N2O cause  CBF w/out dilation. with  production by Lasix and acetazolamide  Enf  production and  resistance to absorption. peds 5.  ICP   CPP. and herniation  All volatile agents  CBF with return to baseline in 3 hrs. with  CMRO2  All volatile agents and kitamine cause cerebral vasodilation.

CXR pneumonia  Pt may present with hymoptysis  required arterial embolization. and restrictive component  And may associated with other condition so look of other underlying disease: aspergillosis. R. and give Abx therapy  Lab: PFT. ABG.Bronchiectasis: Page 62 of 217  Localized irreversible dilation of bronchus  May have COPD. HIV. arthritis  If Pt present to OR with active pul infection postponed Sx. or resection of the affected segment  Consider DLT to isolate the affect lung  Need pre-op Abx .

50% appendix. hypotension. Gentle induction. consider CVP. Histamine. to produce the S/S of the carcinoid syndrome  Could be a manifestation of MEN I. bronchospasm. endobronchial tumor obstruction C Rt side disease  myocardial fibrosis  TR.Carcinoid Tumors Page 63 of 217  GI is the most common source.  hormones secreted by nonmetastatic tumors reach the liver by portal vein and are usually inactivated there. and vasoconstriction . once metastases to the liver. the hormones secreted by the hepatic metastases may have direct access to the systemic circulation. hyperglycemia Intra-op . HTN. STP B bronchospasm. abd pain. also from the lung. diarrhea. 25% in the ileum(the source of metastatic tumors). Kinins  Symptoms: cutaneous flushing. avoid drugs that can cause histamine release octreotide 10-100 ug IV M Dehydration due to diarrhea. V.  Release Serotonin. PR. and hyperglycemia A N/A. art line sympathomimetic drugs can trigger mediator release from carcinoid tumors D Give antihistamines. avoid sux.

o twisting distal trachea (wheezing). o pericardial constriction of the heart (myocardial ischemia and ventricular arrhythmia)  Risks: o Events that  intrapleural pressure in the (ventilated) hemithorax or that  intrapleural pressure in the surgical (empty) hemithorax may predispose the patient to cardiac herniation. in the 1st few hrs or few days later  Pathophysiology: o twisting of the SVC (SVC syndrome). o twisting pulmonary veins (pulmonary edema). o twisting IVC (cardiovascular collapse). And coughing . o Placing the patient with the empty hemithorax in a dependent o Use of high levels of pressure and volume during mechanical ventilation of the remaining lung can push the heart into the empty hemithorax.Cardiac herniation Page 64 of 217  An emergency and life threatening with mortality 50%  With pneumonectomy.

Cardiac Risk* Stratification for Noncardiac Surgical Procedures Page 65 of 217 High (Reported cardiac risk often greater than 5%) · Emergent major operations, particularly in the elderly · Aortic and other major vascular surgery · Peripheral vascular surgery · Anticipated prolonged surgical procedures associated with large fluid shifts and/or blood loss Intermediate (Reported cardiac risk generally less than 5%) · Carotid endarterectomy · Head and neck surgery · Intraperitoneal and intrathoracic surgery · Orthopedic surgery · Prostate surgery Low† (Reported cardiac risk generally less than 1%) · Endoscopic procedures · Superficial procedure · Cataract surgery · Breast surgery *Combined incidence of cardiac death and nonfatal myocardial infarction. †Do not generally require further preoperative cardiac testing.

CAROTID ENDARTERECTOMY Page 66 of 217  Pre-op: H/P  Lab: CBC, Lytes, BUN, creat, Glucose, ECG, PFT if needed A N/A B possible smoker COPD C CAD, HTN (need to well controlled pre-op) M DM CNS neurological deficit  Regional (deep, superficial cervical plexus) Vs GA same out come  Induction: anticipate fluctuation of BP  Maintenance: Iso neuro-protection, Keep BP 20% higher, monitor blood glucose, LA infiltration over the carotid sinus, give heparin 100u/kg  Monitors: standard+ 5leads ECG, Art-line, in cardiac Pt consider TEE, Emergence: early to assess for nay neuro deficit  Post-op potential problems: new neuro deficit back to OR or Angio, hemodynamic instability mainly HTN, bleeding with hematoma formation which may compromise the Airway  Back to the OR, 100% O2 have difficult airway

Canadian Cardiovascular Society Functional Classification of Angina Pectoris 217 Page 67 of Class Definition Specific Activity Scale I Ordinary physical activity, (eg, walking and climbing stairs) does not cause angina; angina occurs with strenuous, rapid, or prolonged exertion at work or recreation. Ability to ski, play basketball, light jog (5 mph), or shovel snow without angina II Slight limitation of ordinary activity; angina occurs on walking or climbing stairs rapidly; walking uphill; walking or stair climbing after meals, in cold, in wind, or under emotional stress; or only during the few hours after awakening; when walking > 2 blocks on level ground; or when climbing more than 1 flight of stairs at a normal pace and in normal conditions. Ability to garden, rake, roller skate, walk at 4 mph on level ground, and have sexual intercourse without stopping III Marked limitation of ordinary physical activity; angina occurs on walking 1 to 2 blocks on level ground or climbing 1 flight of stairs at a normal pace in normal conditions. Ability to shower or dress without stopping, walk 2.5 mph, bowl, make a bed, and play golf IV Inability to perform any physical activity without discomfort; anginal symptoms may be present at rest. Inability to perform activities requiring 2 or fewer metabolic equivalents (METs) without angina

Cesarean Section Page 68 of 217  Depend if elective/urgent Vs stat  Always have the room ready: Anesthesia machine checked, A/W equipment ready, Emergency drugs ready  Always ask for blood for any bleeding case Elective/urgent:  Enough time to evaluate Pt, H/P as routine obstetric Hx, and anesthetic Hx with physical exam mainly the A/W, chest, edema …..+ review lab, obstetric consideration  Obtain informed consent from the Pt for neuroaxial block, with risk/benefit discussion, if not C/I for the block.  Pre-meds  GI, other if indicated e.g. asthma, anxiety, endocarditis, steroids  IV  at least 1.5 -2.0 L of fluids  O2, Pre-block V/S  If using hyperbaric L.A lie the Pt down very quickly + LUD, repeat BP  Inform the Pt that if she feel sick to tell me right way (BP)  Examine the block by asking the surgeon to use a teeth forceps  As soon as the baby out give synto 5 U then 20 U in the bag  For spinal: 10.5 mg marcaine hyperbaric, 20 ug fentanyl, 150 ug epimorph

 VEDP. AICD  Assess using NYHA functional capacity I  no limitation with normal activity. peripheral edema  Rx that proven to improve outcome: ACEI. Rt or Lt  S/S: SOBOE. -blocker. and no symptom II  slight limitation with normal activity. pul HTN  Hallmark: CO. Chem. VHD. CHD. ascites. 12-ECG.CHF: Page 69 of 217  Causes: IHD.  exercise tolerance  P/E: crackles. CXR. symptomatic at rest  Pre-op: postponed if decompensated. les the normal activity produce symptom VI  severe limitation. anticoag. review Echo . comfortable at rest.S3 gallop. PND. SVR. Cardiomyopathy. HTN. vasodilators  Other modality: biventricular pacing. metabolic acidosis  Could be Sys Vs Dias. hepatosplenomegaly.  JVP. spironlactone  Rx that improve symptom: Dig. Cardiology consult to optimize  Workup: CBC. and loop diuretics  Other antiarrhythmics. Lytes. symptomatic III  marked limitation with normal activity. orthopnea.

0 Serum albumin g/100 mL Ascites Encephalopathy Nutrition Prothrombin time (sec > control) Surgical risk mortality rate >3.0 >3.0 2.5 None None Excellent 1–4 5% 3.0–3.0–3.Lab and Clinical Criteria for Estimating Hepatic Reserve (Child-Pugh 70 of 217 Page Classification) CRITERIA CLASS A CLASS B CLASS C Serum bilirubin mg/100 mL <2.5 Easily controlled Minimal Good 4–6 10% <3.0 Not easily controlled Advanced Poor >6 50% .

fib and flutter. kussmaul sign exaggerationin  CVP with inspiration. avoid sudden drop in SVR. radiation. and  stroke volume  Causes: idiopathic. pulsus paradoxes but less than tamponade  CXR: calcification over the pericardium. arthritis. inverted T-waves  Rx  surgical pericardiotomy  Anesthesia Mx o Preload  maintain. since limited CO o Avoid all histamine releasing drugs o Art-line. and avoid .  ECG:  voltage of QRS. since they’re preload dependent o Cont maintain. CRF. CVP at least .  venous pressure. avoid cardio-depressant drugs o Rate: avoid sudden  HR o Afterload maintain. PAC. R. and post-heart  S/S: arrhythmias A.Chronic constrictive pericarditis Page 71 of 217  It resemble tamponade in impede diasolic pressure.

Heart Failure. Death) Major  Unstable coronary syndromes · Acute or recent myocardial infarction* with evidence of important ischemic risk by clinical symptoms or noninvasive study · Unstable or severe† angina (Canadian class III or IV)‡  Decompensated heart failure  Significant arrhythmias · High-grade atrioventricular block · Symptomatic ventricular arrhythmias in the presence of underlying heart disease · Supraventricular arrhythmias with uncontrolled ventricular rate  Severe valvular disease Intermediate  Mild angina pectoris (Canadian class I or II)  Previous myocardial infarction by history or pathological Q waves  Compensated or prior heart failure  Diabetes mellitus (particularly insulin-dependent)  Renal insufficiency .Clinical Predictors of Increased Perioperative Cardiovascular Risk (Myocardial217 Page 72 of Infarction.

aortic rupture or dissection. CVP. avoid sudden  in SVR  Avoid Regional GA is better tolerated for C/S  Monitors  Art-line.  Ephedrine and dopamine are the best choice since they have choronotropic effect . aneurysm of circle of Willis  Measure Rt Vs Lt side BP. and upper Vs lower BP  Need Echo and 12-ECG  hemodynamic Goals: o preload  o R/R  slightly  maintain sinus o Cont  maintain.Coarctation of the Aorta Page 73 of 217  If corrected no special precautions  Arm-leg different < 20mmHg good outcome  Uncorrected high risk of LV failure.  risk of offspring CHD  Risk of having bicuspid aortic valve. endocarditis  High mortality rate. avoid cardiodepressant o Afterload maintain.

DIC. edema. rupture CNS seizure. So consider NTG. CVA fetus  UP blood flow. anemia Hepatic failure.Cocaine abuse Page 74 of 217  Affect three main neurotransmitters Norepi. avoid pure -blockers alone may get unopposed -effect. SAH. bronchspasm. arrhythmias Renal  ARF Heme thrombocytopenia. Serotonin and dopamine  Can present like PIH with HTN. be aware of severe hypotension with spinal. hydralazin with induction. with  risk of coronary vasospasm  Regional OK. pneumomediasinum C MI. proteinuria A B aspiration. ICH.and ephedrine is not a good choice(not work) Neo better . HTN. cross placenta  The main problem is severe HTN with induction. pneumothorax.

acidosis o Respiratory: hypoxia. creat. Neuro GCS. aneurysm. VS. urine analysis.…. encephalitis. LFT.)  H/P AMPLE. DKA. Tylenol. hepatic encephalopathy . Dextrose 50g IV o Lab: ABG. blood/urine for toxicology and drugs level  DDx: o CNS pathology: tumor. . lytes. trauma. coagulation profile. sepsis o Metabolic: hypoglycemia. CBC-D. pupils. seizure disorder. AVM o Infection: meningitis. ECG. uremia. hypercarbia o Overdose: EtOH. BUN. chemostrip. HONKC. Cocaine. drugs(opioids. lateralization.Coma/LOC Page 75 of 217  Management: o ABC o Monitors o Give thiamine 100 mg IV.. TCA.

COMPARISON OF MYASTHENIC SYNDROME ANDMYASTHENIA of 217 Page 76 GRAVIS Myasthenic Syndrome Myasthenia Gravis Manifestations Proximal limb weakness Extraocular. bulbar and (arms > legs) facial muscle weakness Exercise improves with strength Fatigue with exercise Muscle pain common Muscle pain uncommon Reflexes absent or Reflexes normal Gender pathology Response to muscle relaxants Male > female Small cell carcinoma of the lung Sensitive to Sux and NDMR Female > male Thymoma Resistant to Sux Sensitive to NDMR Good response to anticholinesterases Poor response to anticholinesterases .

with spontaneous breathing . N2O C/I.Congenital Diaphragmatic Hernia Page 77 of 217 95% Lt side neonatal and premature consideration A insert NGT . cyanosis. 100% O2 C mediastinal shift  hemodynamic instability .  risk of pneumothorax with PPV. ball valve  avoid PPV. N2O is C/I. keep suction B hypoplastic lung  RDS. 20% CHD Lab X-match Induction gas induction. keep Airway pressure < 20-30 cmH2O. and avoid lung expansion after hernia repair. neonate could be on NO or ECMO. keep 100% O2 C  15% CHD R renal abnormality N neuro abnormality Congenital lobar emphysema o LUL most common o Emergency and potential life threatening A ? B resp failure.

wheezing.  sensitivity to resp depressant drugs Heme polycythemia Lytes   PPC with: FEV1/FVC < 70%. consider Abx therapy  Pt may need O2 supplement pre-op if PaO2<60. FEF25-75 <50%. anticholenergic) . hypercarbia. coughing. A/E bilaterally. PaCO2 > 50  H/P: smoking. Hct >55 . CBC-D. sputum amount and color. pul HTN D avoid STP. bronchospasm. creat  For PFT do pre and post bronchodilators  Optimize the Pt pre-op: smoking cessation. cor pulmonale. BUN. RV failure. ECG. with respiratory failure more likely if FEV1 <50%. steroids. and PPC: atelectasis. pneumonia. ABG. exercise tolerance. crackles. home O2. peripheral edema. wheezing. FVC< 75%. lytes.  JVP. bronchodilators(-agonist. respiratory failure. smoking C cor pulmonale.COPD Page 78 of 217 A  airway reactivity   bronchospasm B  risk of hypoxia. PFT. cyanosis  With smoking  risk of CAD  Lab: CXR.

ST. ST.Coronary Artery Disease— Myocardial Infarction Anatomic Site Leads ECG Changes Inferior II. T Page 79 of 217 Coronary Artery Right Left circumflex Left LAD Electrolyte Disturbances Ca2+ Rate <100 Rhythm Regular PR interval Normal QT interval  Ca2+ <100 Regular Normal/   K+ <100 Regular Normal T flat/U wave K+ <100 Regular Normal T peaked QT  . aVF Q. ST. III. T Anterior I. aVL. T Lateral I. T Anteroseptal V1–V4 Q. V1–V4 Q. ST. aVL. V5–V6 Q.

large tongue. mental retardation  Have a big IV access. TOF. seizure disorder. bear hugger. Foley cath  If involve below the orbit  A/W swelling  keep intubated post-op (ICU) till the swelling subsided . IV wormer . massive blood loss. blood in the OR  If only one suture  short procedure. ICP A possible difficult A/W  maxillary hypoplasia. tracheomalacia.Craniosynostosis: Page 80 of 217  May associated with other syndrome  Crouzon’s syndrome  (MH)  Main issues: difficult A/W. PDA D  Avoid ketamine and sux M  lytes abnormality N  ICP. VAE. multi masks and blads B  tracheal stenosis. OSA C CHD  ASD. CVP. micrognethia Awake FOI. if > 1 . long with risk of bleeding  so need art line.

proteases.Creutzfeldt . formalin. and EEG changes. and extremes of pH. myoclonus. A prion is a small proteinaceous infectious agent. and nucleases. .  incubation time is long (years)  The typical clinical characteristics include subacute dementia. Management of Anesthesia  Because of the transmissibility of the disease. caused by an unusual infectious agent—a prion. Prions are resistant to alcohol. C autonomic dysfunction  abnormal CV responses to anesthesia and vasoactive drugs. Pathologically. but can be inactivated by heat (autoclaving). phenol.Jakob disease Page 81 of 217  human spongiform encephalopathies. A prone to aspirate gastric impaired swallowing function and decreased activity of laryngeal reflexes.  The other two diseases in this group are kuru and Gerstmann-Straussler syndrome. ionizing radiation. these disorders are characterized by vacuolation of brain tissue and neuronal loss. DBecause lower motor neuron dysfunction  succinylcholine should be avoided. appropriate precautions should be taken to protect other patients and health care providers. detergents.

K. cirrhosis. folate M hypovolemia.  3rd space loss. immunosuppressant G obstruction.  albumin   free fraction of drugs MSK arthritis with  ROM . iron def. perforation R amyloidosis Heme chronic anemia. fatty liver.Crohn's Disease Page 82 of 217 A RSI for S/S of bowel obstruction B N/A C hypovolemia D Steroids (stress dose). vit B12.

mucosa easily traumatize B OSA C HTN.05–0. avoid etomidate. volume overload D steroids (stress dose). met alk. K. give 0.1 mg·day–1 of fludrocortisone . and  glucose uptake by the cells  Exogenous therapy (most common) > 21 days  Bilateral adrenal hyperplasia due to ACTH from pituitary adenoma or nonendocrine tumor (lung. 4.maintain BP by converting Norepi  epi. psycosis M  DM. pancreas) A possible difficult A/W. titrate NDMR N  emotional.hyperglycemia by  gluconeogenesis. 3. 2. kidney.antiinflammatory. muscle wasting Immun  infection Post bilateral adrenalectomy may need mineralocorticoid replacement in day 5. and K excretion.Na retention. Addison crisis MSK osteopenia.Cushing Syndrome :( Glucocorticoid Excess) Page 83 of 217  Cortisol function: 1.

CV diseases in pregnancy Page 84 of 217  Lt  Rt shunt e. and avoid spinal  sudden SVR  convert the shunt to Rt Lt o Give O2 all the time . ASD. PDA are well tolerated in pregnancy  The main keys in management for anesthesia are o Avoid air bubble in the IV o For epidural insertion use saline instead of air both due to risk of paradoxical air embolism o Pain   catecholamine   SVR  shunt  RV failure o So early epidural is desirable o Slowly titrate the epidural.g. VSD.

to late diastole Mid-systole y descent Early diastole Early ventricular filling.CVP Waveform Components WAVEFORM a wave c wave PHASE End-diastole Early systole Page 85 of 217 MECHANICAL EVENT Atrial contraction Isovolumic ventricular contraction. systolic collapse v wave h wave x descent Late systole Mid. diastolic collapse . descent of the base. tricuspid motion toward right atrium Systolic filling of atrium Diastolic plateau Atrial relaxation.

 SvO2. which acts as an antidote by converting cyanide to cyanomethemoglobin  hydroxocobalamin (vitamin B12a) which binds cyanide to form cyanocobalamin (vitamin B12) can be administered (25 mg/hour IV to a maximum of 100 mg) . ( converts Hb to methemoglobin. 5 mg/kg. Sz Management:  D/C SNP  100% O2  Thiosulfate 150 mg/kg IV administered over 15 minutes (acts as a sulfur donor to convert cyanide to thiocyanate)  If severe. with deteriorating hemodynamics and metabolic acidosis  slow IV administration of sodium nitrate. tachyphylaxis to SNP.Cyanide toxicity Page 86 of 217  By preventing oxidative phosphorylation cellular hypoxia anaerobic metabolism  S/S lactic acidosis.

hepatic dysfunction Heme bleeding disorder  Lab: CBC-D. Abx. CXR. art-line  Suction the airway before extubation  Consider regional block for post-op pain control  Encourage chest physio post-op .Cystic fibrosis: Page 87 of 217  A disease of the exocrine glands: salivary. GI enzyme A sinusitis  avoid nasal intubation with active nasal infection. lytes. pul  Rx: chest physio. bronchodilator. bronchiectasis C cor-pulmonale GI cholelithiasis. creat. PFT. GI. BUN. B pneumonia. mixed obstructive/restrictive disease. sweet. Echo if needed  Monitors: CAS. pancreatic insufficiency. coags. ECG.

if abnormal renal functionhydroxocobalamin o NTG: less potent.Deliberate Hypotension: Page 88 of 217  Mainly used to  blood loss: aneurysm. risks:  pul shunt. Esmolol and Labetalol. hypoxia. cyanide and thiocyanate toxicity.  CMRO2.g. 70% of the awake MAP  Monitors: Art-line. acidosis.5mg/kg in 24hrs. o Isoflurane: easy titration. heart failure. CVP.  ICP. spine Sx. Prostaglandin E1. also it’s inhibit PLT aggregation. but  shunt. Renal insuff  Ass intravascular volume pre-op. major head and neck  The main C/I are: uncontrolled HTN. or 0. resp failure. and rebound HTN. TIA’s angina. Nicardipine . AVM. Rx of toxicity: IV thiosulfate. no cyanide problem. o Other: Trimethaphan. and expand it if necessary. or > 1mg/kg in 2hrs. severe anemia. SSEP or EEG in brain and spine Sx  Choices: o SNP: rapid on/off. do not exceed 10ug/kg/min for 10 min.  Have a target MAP based on awake MAP e.

 As a consequence of the large outpouring of ADH in response to surgical stress. and a high output of poorly concentrated urine.  DDAVP administered intranasally has prolonged antidiuretic activity (12– 24 hours) and is associated with a low incidence of pressor effects.Diabetes Insipidus Page 89 of 217  from inadequate secretion of ADH (central DI)  or resistance on the part of the renal tubules to ADH (nephrogenic DI)  Failure to secrete adequate amounts of ADH results in polydipsia. The serum sodium and plasma osmolality are measured on a regular basis. the patient with complete DI receives an iv infusion of aqueous ADH (100–200 mU·h–1) combined with administration of an isotonic crystalloid solution. patients with a residually functioning gland usually do not need . management  depends on the extent of the hormonal deficiency. and therapeutic changes are made accordingly. During surgery. or surgery. Etiology  due to destruction of the pituitary gland by intracranial trauma.  ADH also may be given intramuscularly (as vasopressin tannate in oil). hypernatremia. infiltrating lesions.

full stomach M hypo. DKA. autonomic neuropathy. Lytes. cardiomyopathy . BUN. hyperosmolar coma Renal  renal function CNS neuropathy (positioning). Art-line.DIABETES MELLITUS Page 90 of 217 A stiff joint syndrome ―prayer sign.  mobility of the AO joint.‖. frequent ABG. difficult intubation. postponed DKA. hyperglycemia.  risk of post-op MI D metformin associated with lactic acidosis in hypotension. creat  D/C OHA in AM. FBS. includes 5-leads ECG. consider insulin/D5% infusion peri-op for long cases  Document neuropathy pre-op for positioning and regional anesthesia  monitoring intra-op. silent MI. or chemosrip for glucose. lytes abnormalities. RSI  full stomach B N/A C CAD. and in PARR  unless it’s an emergency Sx. and hyperosmoalr coma . CVA  Pre-op: lab: ECG. hypoxia GI delayed gastric emptying. PVD. FOI.

Diabetic Ketoacidosis Page 91 of 217  Accumulation of acetoacetate and -hydroxybutyrate  ketone bodies are organic acids metabolic acidosis with an unmeasured AG.  Provoked by intercurrent illness, trauma, or cessation of insulin therapy.  the degree of hyperglycemia does not correlate with the severity of the acidosis.  Blood sugar levels are often in the 300–500 mg·dl–1 range.  leukocytosis, abdominal pain, GI ileus, and mildly  amylase levels are all common in DKA, Pt may Dx as acute abdomen. Treatment  Regular insulin 10 units iv bolus followed by an insulin infusion nominally at (blood glucose/150) units·h–1  Isotonic iv fluids as guided by V/S and urine OP; anticipate 4–10 l deficit  When urine >0.5 ml·kg–1·h–1, give KCl 10–40 mEq·h–1 (with continuous ECG)  When glucose  to 250 mg·dl–1, add dextrose 5% at 100 ml·h–1  Consider sodium bicarbonate to correct pH <7.1  When glucose levels  below 250 mg·dl–1, glucose should be added to the iv fluid while insulin therapy continues.  K replacement is a key concern in patients with DKA, Because of the diuresis, the total body potassium stores are reduced.


Page 92 of 217

Dilated Cardiomyopathy  myocardial contractility systolic dysfunction CO ventricular filling pressure  Dilatation of both ventricles MR, TR.  Causes: the most common is IHD and alcohol  Other causes: o Direct:  Toxic :Alcohol, Anthracyclines, Catecholamines, Cobalt, Phenothiazines, Radiation, Uremia, Adriamycin.  Infectious:Protozoan (Chagas' disease) Viral (coxsackievirus, other enteroviruses, influenza)  Metabolic :Starvation, Thiamine deficiency (beriberi)  Genetic, Idiopathic o Indirect  Ischemic  Large-vessel coronary disease (postinfarction cardiomyopathy)  Small-vessel coronary disease  Global ischemia (cardiac surgery)  Anemia, TTP, Hypersensitivity, Idiopathic myocarditis

Down syndrome: Page 93 of 217  Highly associated with CHD 50%, cyanotic 8%(mainly TOF) A C1-2 subluxation, subglottic stenosis, large tongue  difficult intubation, avoid neck extension B C CHD, TOF, CHF, Tet spells, Rt Lt shunt ( be meticulous about air in the IV) M hypothyroidism, hypothermia CNS MR

ECT during pregnancy  Obstetric consideration   Risk of abortion and premature labor, also  risk of bleeding  Minimize the amount of drugs as much as possible  Use only the drugs that are known to be safe(STP, Sux, NDMR, Opioids, Ketamine, Etomidate)  Have an obstetric consultation  Beyond the 1st trimester do GA with ETT, RSI, with maintaining LUD  Have FHR monitor

EEG FREQUENCY RANGES Page 94 of 217 Delta rhythm (0–3 Hz)  Deep sleep, deep anesthesia, or pathologic states (e.g., brain tumors, hypoxia, metabolic encephalopathy) Theta rhythm (4–7 Hz)  Sleep and anesthesia in adults, hyperventilation in awake children and young adults Alpha rhythm (8–13 Hz)  Resting, awake adult with eyes closed; predominantly seen in occipital leads Beta rhythm (>13 Hz)  Mental activity, light anesthesia Effect of anesthesia is depend on the dose. @ low dose  frequency @ moderate dose  frequency and  amplitude @ high dose  silent compare to SEP, EEG records the spontaneous brain activity with higher amplitude, while the SEP have a smaller amplitude in response to a specific stimuli.

consider SBE prophylaxis Heme bleeding disorder with normal coags profile  Anticipated problem  bleeding  Obstetric  premature labor & bleeding  Avoid Regional Anesthesia Page 95 of 217 . Arrhythmias. Avoid high airway pressure C MR.Ehlers-danlos Syndrome:  CTD. abnormal metabolism of type III collagen A avoid A/W traumatization B spontaneous Pneumothorax.

with pads on the Pt  Epidural have better outcome than GA careful titrate LA Page 96 of 217 . O2 all the time. demise  high rish of thromboembolic event mainly post partum  Hemodynamic Goals: o preload maintain.  PCO2  Consider inhaled NO. avoid cardiodepressant o Afterload maintain. PAC/CVP  For the 1st stage  single shot spinal opioids  2nd stage may consider slow titrating epidural  Be aware that they could be anticoagulated  For C/S crash cart in the room.Eisenmenger Syndrome  Chronic Lt Rt shunt changes to Rt Lt  Pregnancy  S/S due to  SVR  hypoxia IUGR. acidosis. avoid sudden  in SVR o PVR  avoid  by hypoxia. avoid AC compression  LUD o R/R  maintain normal sinus o Cont  maintain. with pulse oxi  Monitors  Art-line.

and other injuries o Potential burn to the face  early intubation . current pathway.Electric shock and lightning strike Page 97 of 217  Electric shock o Direct effect of the current o Conversion of electric to heat energy  Factors determine the nature and severity: magnitude of energy delivered. muscle. tetanic contraction of resp muscles. type of current. nerve have a low resistance o The skin resistance can be  by moist  and convert a low voltage to a life threatening shock o Alternating current is more dangerous than a direct current o Transthoracic (hand-hand) are more dangerous than vertical ones o VF more common with alternating. resistance to current. while asystole more with direct o Respiratory arrest due to CNS effect (medulla). and prolonged paralysis o Consider C-spine precaution. and duration of contact o Bone and skin have a high resistance o Blood vessels.

or innocent heart murmurs . including bioprosthetic and homograft valves  Previous bacterial endocarditis  Complex cyanotic CHD (eg. TGA. functional. single ventricle states. rheumatic heart disease)  Hypertrophic cardiomyopathy  Mitral valve prolapse with valvar regurgitation and/or thickened leaflets Endocarditis prophylaxis not recommended Negligible-risk category (no greater risk than the general population)  Isolated secundum atrial septal defect  Surgical repair of ASD. or PDA (without residua beyond 6 mo)  Previous coronary artery bypass graft surgery  Mitral valve prolapse without valvar regurgitation  Physiologic.Cardiac Conditions Associated With Endocarditis Page 98 of 217 Endocarditis prophylaxis recommended High-risk category  Prosthetic cardiac valves. TOF)  Surgically constructed systemic pulmonary shunts or conduits Moderate-risk category  Most other congenital cardiac malformations (other than above and below)  Acquired valvar dysfunction (eg. VSD.

5 kg  Allergy to Amp Vanco and Gent. Peds 20mg/kg  GU/GI o High risk: Amp & Gent  Adult 2g/ 1. oral.Endocarditis Prophylaxis  Dental. esophageal. 1g for adult and 20mg/kg for peds o Moderate risk: Amp alone  Same as above dose  Allergy to Amp Vanco also the same dose Page 99 of 217 .5/kg max 120mg  Peds 50mg/kg & 1. and respiratory o Adult: Ampicillin 2g IV 30 min pre-op o Peds: Ampicillin 50mg/kg within 30 min of starting o Allergy to Amp  Clindamycin 600 mg .

 3 types o simplex benign o junctional rarely survive beyond early childhood o dystrophic. avoid tourniquet.Epidermolysis Bullosa Page 100 of 217  inherited or acquired  loss of intercellular bridges and separation of the skin layers intradermal fluids accumulation and bulla formation. cardiomyopathy o CVS: cardiomyopathy and MVP o Lytes: loss of albumin hypovolemia and electrolytes imbalance o Associated diseases: D.  Systemic manifestations and Anesthetic considerations: o A very fragile m.m bledding & bulla formation with fixation of the tongue difficult intubation use a lot of lubricant on the ETT. BP cuff must be pad with cotton o GI: esophageal stricture malnutrition anemia. multiple myoloma .M. and avoid suctioning o skin: very fragile avoid tapes for IV and ETT. hypercoagulation. porphyria cutanea tarda.

Epiglottitis Page 101 of 217  an emergency and life threatening condition  1-7 y. and the kid is sitting foreword. and need to be kept intubated for 24-72h. inspiratory stridor. in the presence of the ENT surgeon in the room. with Abx therapy  After intubation risk of pul edema  NO NO NO muscle relaxant  Give atropine . high grade fever. with toxic appearance  Need to managed in the OR. and have different sizes ready  After Intubation keep sedated and transfer to ICU. and the difficult airway cart in the room  Do a gas induction with Sevo. with  incidence due to vaccine  The main conflict is difficult airway with risk of aspiration  Other DDx is retropharyngeal abscess  Rapid onset within 24h. influenzae. mouth opening and drooling. and maintain spontaneous ventilation  Use a smaller ETT.o. keep the kid with the parents. and do a gas induction without starting an IV. most common pathogen is H.

bleeding). tumor. .Epilepsy: Page 102 of 217 H/P: why(pathology: head injury. dose. avoid any drugs that may  seizure threshold. drugs effect (cardiotoxicity) D  resistance to NDMR with phenytoin. hepatic toxicity with carbamazepine. CVA. enzyme induction with pentobarb. frequency. to be taken in AM A N/A B possible frequent aspiration C tuberous sclerosis. S/S of  ICP Meds: what. last aepisode. type. other: aplastic anemia.

and keep communication with Pt all the time  In case of A/W obstruction D/C sedation gtt. mainly anticonvulsant   metabolism of NDMR  Discuss with the surgeon the anesthetic plan GA Vs sedation with LA  May need awake test with speech mapping  In case of sedation use a judicious amount of sedation.Epilepsy surgery Page 103 of 217  Hx  type generalized. or without Aura  Review all meds. also avoid any long acting anticonvulsant . 100% O2 LMA. Rt temporal Rt radial art line  Avoid any pre-med that may change the seizure threshold. ETT  In addition to the standard CAS monitoring. absence. focal. with.g. if an Art-line needed have in the same side of the lesion e. O2 by NP.

Sz. tetany o II (12-24hr) Cardioresp HTN. Lytes. Lytes Ca o Gastric lavage o Depend on the serum level of EG whether to give EtOH or not or to start HD . ABG. ECG o Monitors: ECG. pul edema o III (24-72hr) Renal flank pain. BUN. pulse oxi. EG level. and osmolar gap  S/S depend on when they present and at which stage: o Stage I (30min-12hr) CNS with hallucination. polish  The toxic metabolite Glycolic acid is responsible for the metabolic acidosis with anion gap. Osmolality.Ethylene Glycol poisoning Page 104 of 217  Found in: detergent. tachycardia. creat. coma. Foley cath o ECG QT. CXR. art-line. antifreeze. Ca oxalate in the urine  Management: o ABC o Lab: CBC-D.

metabolic acidosis.  evidence of myotonia as well as episodes of muscle weakness.  Episodes of weakness lasting several hours can occur: during rest after exercise. .Familial Periodic Paralysis Page 105 of 217  Two forms: hyperkalemic.  K levels measured during the episode of weakness may be N or even   Treatment consists of a low-K diet and the administration of thiazide diuretics.  hyperkalemia is often transient. Hypokalemic Periodic Paralysis.  Consider glucose containing solution pre-op during fasting. infusions of KCl.  The weakness may be so severe as to produce respiratory distress. Attach may last hours or days.  caused by a sodium channel mutation. caused by a calcium channel mutation. acute episodes of skeletal muscle weakness. both AD inherited diseases. or hypothermia.  More common. and hypokalemic.  intermittent. occurring only at the onset of weakness. Hyperkalemic Periodic Paralysis.

4)  CNS depression (disproportionate to hypoxemia)  Pulmonary edema o MINOR  Tachycardia (>110 beats·min–1)  Hyperthermia  Retinal fat emboli  Urinary fat globules   platelets/hematocrit (unexplained) . and the mortality rate ranging from 10 to 20%. rheumatoid arthritis. intramedullary instrumentation.  The incidence of FES in isolated long bone fractures is 3–4%.Fat Embolus Syndrome Page 106 of 217  associated with multiple traumatic injuries and surgery for long bone #  Risk factors include:male sex. FIO2 < 0. hypovolemic shock.  CRITERIA FOR DIAGNOSIS OF FAT EMBOLUS SYNDROME o MAJOR  Axillary/subconjunctival petechiae  Hypoxemia (PaO2 < 60 mm Hg. age (20–30 years).

Flow volume loop Page 107 of 217 .

9% severe  Clinical signs Mild mod severe Urine   anuria Mucosa slight dry Dry parched Fontanel N sunken marked sunken Eye N sunken marked sunken . and the rest in the nest 2 hrs  Glucose requirement for neonate 4-6 mg/kg/min  D10W 100mg/ml of glucose  Dehydration o Based on body wt in infant 5% mild. 10% mod.Fluids Page 108 of 217  Blood volume o Preterm 100 ml/kg o Newborn 85 ml/kg o Up to 2y 75 ml/kg o 2-puberty 70 ml/kg  Maintenance use the rule 4-2-1. add the deficit using the same rule from NPO and replace it 50% in the first hr. 6% mod. 15% severe o >15 kg 3% mild.

DKA. BUN. R renal dysfunction Fetus/neonate  hypoglycemia. ABG (PRN) Pre-med GI. Lytes. ECG. Creat. hypothermia. Review White classification for DM its according to the severity Page 109 of 217 . ANS dysfunction hypotension with R. lethargy Lab: CBC-D. HNKC CNS ANS dysfunction.  risk of C/S  In addition to obstetric consideration A Stiff joint syndrome difficult A/W B C hypovolemia.Gestationl diabetes   maternal/fetal M/M.  bili.anesthesia D insulin M hypoglycemia.

LMN involvement ? caused by viral infection GI. ECG. CXR. stimulator in place  Post-op: continue mech vent (ICU)  In Pt with previous disease assess for residual neuropathy. have N. Lytes  Before induction have an art-line in place.  sensitivity to NDMR GI bowel obstruction CNS  demyelination  Pre-op: PFT. difficult intubation if TMJ involvement B respiratory involvement C arrhythmia. avoid Spinal  severe hypotension . unpredictable response to intubation and induction. consider CVP. autonomic dysfunction D NO Sux.Guillian barre’ Syndrome Page 110 of 217  Widespread inflammatory demyelination of peripheral and ANS  It’s ascending in nature. (K). flu A full stomach. ABG. epidural OK. and do PFT  In pregnancy  premature labor. CBC.

art line.25-1g/k. or DAI. PCO2 30. the secondary is an exacerbation of neuronal damage from change in CBF. use lido. CVP. adequate pain/sedation. Lytes.g. CBC. hypoxia. contusion. hypothermia  Anesthesia goals: o Optimize CPP. pupils.Head and spinal cord injury Page 111 of 217  15% of CO to the brain. temp . focal/lateralization neuro signs  Lab: CT-head. avoid CMRO2  Exam: GCS. BP. severe  PCO2. but PCO2 reactivity is preserved with  in magnitude.  Monitors: routine. avoid ischemia.  temp. sux . Coags. it’s very important to maintain SBP > 90   ICP  maintain O2. avoid drugs/tech  ICP. with CBF of 50ml/100g/min  Pathophysiology:  TBI primary injury is due to hematoma. inline stabilization. anemia. and systemic factors e. mannitol . adequate cerebral drain head up. and herniation  The Autorgulation of CBF is disrupted. toxicology screen  Induction: RSI. ICP. Sz  Hypotension is the most important factor  poor prognosis  The effect of  ICP   CPP. brainstem reflex.

Table 25-4.0136 g-m·beat–1·m–2 . DERIVED HEMODYNAMIC VARIABLES Name Calculation Units CI CO/BSA l·min–1·m–2 SVR (MAP-CVP/CO) X 80 dyne-cm·s–5 PVR (MPAP-PCWP/CO) X 80 dyne-cm·s–5 Stroke index SI CI/heart rate cc·beat–1·m–2 Page 112 of 217 Left ventricular stroke work index :LVSWI SI X (MAP-PCWP) X 0.0136 g-m·beat–1·m–2 Right ventricular stroke work index :RVSWI SI X (MPAP-CVP) X 0.

Hemophilia Page 113 of 217  A deficient or functionally defective Factor VIII:C.  Lab:  PTT. and the dose of factor VIII:C need to be  . avoid Regional anesthesia . VIII t1/2 is 12 hrs. avoid blind suctioning. Hemophilia C is an AR disorder that occurs almost exclusively in Ashkenazi Jews  Normal concentration of vWF. with normal BT. also DDAVP  factors release from the endothelium  With time type A may develop inhibitors to factor VIII:C . (85%)  B (Christmas disease)  deficiency or abnormality of Factors IX(14%)  C  deficiency or abnormality of Factor XI (1%)  Both hemophilia A and B are sex-linked recessive disorders. with N PT. Hematology consult  Rx factors concentrate VIII. which therefore occur almost exclusively in males. may give Cryo if needed. direct relation between the severity of bleeding and the plasma concentration of the factors  CNS bleed is the major cause of death. IX and XI. IX is 24 hrs. Possible HIV +  Do gentle intubation.

lytes abnormality. lytes. PLT. fibrinogen). PTT. B hypoxemia due to shunt. Echo. Cryo. creat. with  Post-op M&M  Risk of transmission to OR personal (use needle-less system) A RSI for GI bleeding. acidosis Renal hepatorenal syndrome GI portal HTN. coagulation defect M  albumin. ascites. restrictive lung disease.C. Page 114 of 217  Depends on the activity and the stage. Vit K)  Consider paracentesis pre-op if respiratory compromise  Have an ICU consult and back-up bed  Lab: CBC-D. BUN.Hepatitis B. LFT. hypoglycemia. CXR. ABG . upper GI bleed CNS encephalopathy  Correct coagulation pre-op (FFP. PFT. ECG. coags(PT. CHF D altered drug pharmacokinetics Heme anemia. Pul HTN C hyperdynamic circulation. PLT.

pancreatitis. autonomic neuropathy D drugs related side effect neuropathy. HBV . myocarditis. dehydration. drugs  Possible substance abuse cocaine. heroin. anemia. opioids . adrenal insufficiency CNS demyeliantion neropathy like gullian barre’ syndrome R+ Lytes CRF from sepsis. TB.HIV Page 115 of 217  The main considerations are the disease process. hypoxia. pul HTN. ARDS like. side effect of antiviral drugs. endocarditis. ITP Endo DM. diarrhea Heme leukopenia. and health care personal safety A N/A B PCP. pericarditis. other infection HCV. lactic acidosis. C accelerated CAD. and the protease inhibitor may interact with cytochrome P-450 either by induction or inhibition which can  sensitivity to BNZ GI esophagitis.

avoid sudden  in SVR  Neo is the drug of choice if BP  Epidural  very slow titration  With GA risk of CHF Page 116 of 217 . give slowly  hemodynamic Goals: o preload . LUD o R/R   maintain sinus.HOCM  With pregnancy  HR and contractility with  SVR  worsen the obstruction  -blockers is the treatment of choice  Synto  no bolus. avoid  contractility (kitamine) o Afterload . treat arrhythmia aggressively o Cont  .

Rt shift of auto regulation curve  Hydrate pre-induction  Consider Art-line depend on Pt status and the procedure  Lab ECG. PVD. Lytes. LVH.  With secondary look for the underlying cause: cushing. with labile BP M  intravascular volume R renal impairment CNS TIA. …. BUN. pheo.HTN  Essential or secondary. creat Page 117 of 217 . CVA. and 2-agonist peri-op  D/C ACEI A N/A B N/A C CHF. CBC.  Postponed if DBP > 110  Continue -blockers. HTN.

or LP shunt.  LOC  The rest of management as  ICP card Page 118 of 217 . VA.Hydrocephalus:  Etiology: o Trauma/hemorrhage  IVH o Congenital Arnold-chiari malformation o Neoplastic tumor o Post-inflammatory sbscess. HTN) D avoid ketamine and sux N   ICP. A impaired A/W reflex  aspiration RSI B impaired resp drive  ABG C Cushing reflex (brady. meningitis  Pt may come for VP.

cerebral edema is a risk.  One to 2 L of NS. .Hyperosmolar Nonketotic Coma Page 119 of 217  In type II (NIDDM)  elderly patient with minimal or mild diabetes may present with remarkably high blood glucose levels and profound dehydration.  enough endogenous insulin activity to prevent ketosis.  responds quickly to rehydration and small doses of insulin.  Insulin. and recovery of mental acuity may be delayed after the blood glucose level and circulating volume have been normalized.  it is the combination of an impaired thirst response and mild renal insufficiency that allows the hyperglycemia to develop.  with the increased plasma viscosity producing a tendency to intravascular thrombosis. or equivalent. by bolus or infusion.  The marked hyperosmolarity may lead to coma and seizures. infused over 1–2 hrs if there are no cardiovascular contraindications.  Consider NaHCO3 if severe acidosis  With rapid correction of the hyperosmolarity. even with blood sugar concentrations of 1000 mg·dl–1. should be administered. they are not in ketoacidosis.

Hyperparathyroidism Page 120 of 217  Primary benign parathyroid adenoma (90% of cases) or hyperplasia (9%) and very rarely to a parathyroid carcinoma. .  Pregnant women with primary hyperparathyroidism should be treated with surgery.e. CRF.  occurring during pregnancy is associated with a high maternal and fetal morbidity rate (50%).  Surgery is the treatment of choice for the patient with symptomatic disease. malabsorption  Tertiary  development of hypercalcemia in a patient who has had prolonged secondary hyperparathyroidism that has caused adenomatous changes in the parathyroid gland and PTH production to become autonomous.  Secondary in parathyroid function as a result of conditions that produce hypocalcemia or hyperphosphatemia. promoting fetal hypercalcemia and leading to hypoparathyroidism in the newborn. The placenta allows the fetus to concentrate Ca. or as part of a (MEN) syndrome.  most Pt are hypercalcemic. most are asymptomatic at the time of diagnosis.g.

PLT  Consider giving -blockers peri-op. between the ages of 20 and 40 years and is predominant in women A potential difficult if large goiter B N/A C hyperdynamic.Hyperthyroidism Page 121 of 217  most common etiology is the multinodular diffuse goiter of Graves' disease. HTN D Avoid ketamin. and  the conversion of T4 to T3 . to  HR. and pancuronium M  Ca Heme anemia.

MR is common  Could be dynamic obstruction by the anterior leaflet of the MV during systole systolic anterior motion (SAM).  CCB is other choice. F>M.fib systemic embolism  Atrial kick very important A.Hypertrophic Cardiomyopathy Page 122 of 217  AD.CHF  A. Syncope. S/S  Angina. diuretics hypovolemia  obstruction.fib not well tolerated  CXR Cardiomegaly  ECG LVH Treatment:  -blockers 1st choice by  HR and contractility  outflow obstruction. HTN is a common cause. . Good EF due to hypercontractile state. Peak 5th decade of life. Could associated with LVOFO or without  Sport  sudden death. Arrhythmia.  CHF is difficult to treat digoxin  contractility  obstruction.

use the following equation: Current [Na+] × current TBW = desired [Na+] × desired TBW TBW= 0.Within 3 to 4 weeks of the clinical onset of the syndrome. Also treat the underlying causes To calculate the net water loss necessary to  [Na+] in hyponatremia. so it’s result from excess or deficit of water  total body Na regulated by aldosterone and ANP. tumor. risk head trauma. cerebral hemorrhage and CHF  Once serum Na > 120 fluid restriction is enough . mediated by BNP. SAH. areas of demyelination are apparent on MRI. and infection  SIADH  see other card  Rx < 120 with 3% NS @ 1-2 ml/kg/hr to  serum Na 1-2 mEq/l/hr only for few hrs. poor nutritional status.6x wt . cramps. independent of SIADH. weakness. not more than 25 mEq/l/48 hrs  Rapid correction  abrupt brain dehydration central pontine myelinolysis mild (transient behavioral disturbances or seizures) to severe (including pseudobulbar palsy and quadriparesis). risk factors (alcoholism. LOC. where serum [Na] by ADH  S/S depend on the rate and severity of  of Na: loss of apatite. N&V. and hypokalemia) . coma and seizure  Acute CNS S/S is due to cerebral edema  What is the serum osmolality see figure  Cerebral salt wasting syndrome. liver disease.Hyponatremia < 130 Page 123 of 217   or  in serum Na   &  in ECV & PV. burns.

or an infiltrating process (malignancy or amyloidosis).Hypoparathyroidism Page 124 of 217  underproduction of PTH or resistance of the end-organ tissues to PTH results in hypocalcemia  normally: hypocalcemia PTH and 1. granulomatous disease.  Pseudohypoparathyroidism is an inherited disorder in which parathyroid gland function is normal but the end-organ response to the PTH is deficient.  Affected patients have hypocalcemia and hyperphosphatemia.  most common cause of acquired PTH deficiency is inadvertent removal of the parathyroid glands during thyroid or parathyroid surgery.  They are characterized by mental retardation. and shortened metacarpals. obesity.  Chvostek's sign is a contracture of the facial muscle produced by tapping the facial nerve as it passes through the parotid gland. neck trauma. adrenal insufficiency). GI absorption. and renal tubule reclamation. .  Idiopathic is rare and may occur as an isolated disease or as part of an autoimmune polyglandular process (hypothyroidism. a short stature.25(OH)2D synthesis  Ca2+ mobilization from bone.  Other : 131I therapy for thyroid disease.

Hypotension Preload:  Hypovolemia  Venodilation (spinal)  Tamponade  Tension Pneumothorax R&R:  Too fast and too slow  Arrhythmias Other (may affect any component):  Electrolytes imbalance  Acid-base  Hypoxia & hypercarbia Contractility:  Ischemia  Valve dysfunction  CHF  Drugs Page 125 of 217 Afterload:  Drugs  Anaphylaxis  Sympathectomy  Hyperthermia  sepsis .

edema GI  gastric emptying  aspiration M Na. . hypoparathyroidism. pul edema C bradycardia. hypoventilation. DM.  response to PCO2 and PO2. hypotension. CHF.  sensitivity to narcotics.  Consider adrenal insufficiency when intra-op hypotension not responding to fluids and inotrops. heart block. RA. A goiter  altered A/W anatomy. Addison’s disease. possible SIADH. possible Addison’s disease  postponed if severe hypothyroid Pt until at least partially treated.  Maintain normal body temperature. thyroid replacement should probably be delayed until after coronary revascularization.g. with possible A/W obstruction B OSA.  The management of hypothyroid patients with symptomatic CAD has been a subject of particular controversy. hypothermia.  May associated with amyloidosis.Hypothyroidism Page 126 of 217  Hashimoto’s thyroiditis may associated with other autoimmune disease e. SLE. In symptomatic patients or unstable patients with cardiac ischemia.

MI  (ECG.5-1.hyperventilate PaCO2 25-30 good only for 6 hrs 2. avoid PEEP if possible . artline. CVP Mx: 1. Lasix 0.Barbiturate 6.CSF drain  Avoid neck twisting obstruction of IJ.  LOC. ICP: Page 127 of 217  Normal ICP < 10 mmHg. risk of herniation M  DI.0 mg/kg 3. Echo) D  avoid sux N   ICP. hemodynamic instability.32 A   LOC.diuretics mannitol 0.head elevation 5. cerebral salt wasting Monitors: routine. SIADH.Steroids  need 6-24 hrs to work 4. avoid hyperglycemia  Maintain CPP. MAP > 60. aspiration risk B  resp failure C arrhythmias. ICP.25.1. to convert to cmH2O X by 1.0 g/kg over 10 min.

synto OK  Need continues sat and ECG monitor  Epidural is good prevent  catecholamine and hyperventilation which  PCO2  coronary vasospasm  Neo is a better choice  Epidural best for C/S .IHD Page 128 of 217  Apart from atherosclerotic disease. cocaine abuse  Avoid ergot. pheo. sickle cell disease. PIH. other causes are: collagen vascular disease.

Kell. Kidd.Immediate Hemolytic Transfusion Reactions Page 129 of 217  Catastrophic and life threatening with mortality 20-60%  Hemolysis of the donor RBC  ARF. inotrops  Preserve renal function diuretics. N&V. Lewis. direct coombs test ( for definitive diagnosis) . chills. death  Intravascular and extravascular (RES)  Antibodies anti-A. and anti-Duffy  Ag-Ab complex  activate Hageman factor(XII) kinin bradykinin   capillary permeability. flushing.  bleeding. hypotension. Hemoglobinuria  Management: (keep index of suspicion) o Stop Tx.B. maintain BP. rigor. prevent stasis o Blood sample should be collected in EDTA tubes for re-X match. alk the urine (NaHCO3)  Prevent DIC  no specific therapy. chest and abdominal pain  Under GA most of S/S are masked only hypotension. tachy. also complement  histamine . tachycardia. serotonin  S/S: fever. o 3 main objectives:  Maintain BP  volume. diarrhea. re-check blood. DIC.

Massive hemorrhage 2. Control of distribution of ventilation to only one lung a. Unilateral lung lavage 4. Major bronchial disruption or trauma 3. Middle and lower lobectomy c. Isolation of each lung to prevent contamination of a healthy lung a. Video-assisted thoracoscopic surgery RELATIVE 1. Esophageal surgery b. Infection (abscess. Unilateral cyst or bullae d. Upper lobectomy 2.INDICATIONS FOR ONE-LUNG VENTILATION ABSOLUTE 1. Pneumonectomy c. Thoracic aortic aneurysm b. Surgical exposure—low priority a. Thoracoscopy under general anesthesia Page 130 of 217 . Bronchopleural fistula b. Surgical exposure—high priority a. infected cyst) b. Bronchopleural cutaneous fistula c.

arrhythmias ST-changes .Infratentorial Intracranial Tumors Page 131 of 217  Those tumors produce a mass effect on the brain stem. risk SC compression Prone  see other card  Monitors as Supratentorial tumors  Induction also the same  Post-op: o need for continuous CV monitoring 24-48 hrs o HTN is a common problem post-op. XII  loss pharyngeal sensation  may need to keep intubated . HTN. and  ICP by obst hydro A CN involvement +  LOC  unprotected A/W RSI B Resp depression C brady. CV instability in elderly. X.  LOC Position sitting  risk of VAE . need to treated aggressively  other wise  intracranial bleeding and edema o Manipulation of CN IX. prolonged QT CNS ICP.

ITP Page 132 of 217  More common in young female. IVIG. HIV. where major cause of mortality is intracranial bleed  The main ttt is steroid. plasmaphoresis. DIC. essential thrombocytopenia  The main issues with Anesthesia Are o A avoid traumatize the airway o Avoid Regional o Risk of bleeding  PLT Tx  In Preg  antibodies cress the placenta  affect the fetus  CNS bleed  C/S TTP  It’s: thrombocytopenia. drug induced thrombocytopenia. characterize by thrombocytopenia with petechiae. and jaundice  ttt  Tx plasma. other in preg  PIH. hemolysis. renal dysfunction. fever. CNS involvement Sz. steroids  also the same issues as ITP regarding anesthesia . Connective T disease. if not working  splenectomy  Consider DDx: TTP.

Lytes. and diuresis with lasix. CVP  Goals  maximize the renal perfusion at the time of graft reperfusion by maintaining a high BP. arrhythmias D altered drugs pharmacokinetics G Gastroparesis M  K. Art-line. BUN. secondary hyperparathyroidism with  Ca and  phos Heme PLT dysfunction secondary to uremia  Lab CBC-D. pericarditis.  intravascular volume. CXR. and mannitol  Possible problem Bleeding  Post-op pain  epidural. X-match  monitorsCAS. creat. PCA . foley. pericardial effusion. ECG.Kidney Tx Page 133 of 217  Of course for CRF A RSI for possible gastroparesis B pul edema if volume overloaded C hyper/hypovolemia.

with no sensory deficit Femoral N:  Due to pelvic Sx. external rotation during the 2nd stage of labor. prolonged hip flexion. numbness. with loss of ankle dorsiflexion  L5 dermatome loss of sensation lateral leg  In obstetric  with prolonged labor and difficult vaginal delivery Obturator:  Weakness of hip adduction and internal rotation Peroneal N  With prolonged lithotomy position  At the knee level (injury) foot drop. with loss of the patellar reflex Meralgia paresthetica(Lateral femoral cutaneous nerve)  tingling. as well as lithotomy position  Walking OK. burning sensation over the lateral thigh  resolve spontaneous after giving birth .Lower Ext nerve inury: Page 134 of 217 Lumbosacral trunk:  Foot drop. abduction. but unable to claim stairs.

pericarditis  Have the ENT surgeon in the room. submental. Pneumothorax. pericarditis. consider a reinforced and small size ETT  Awake FOI. fever. effusion. give glycopyrolate. inability to open the mouth. causing empyema. difficult A/W B hypoxia. pericardial effusion. and sublingual  Early S/S: chills. involves 3 fascial spaces: submandibular. including gas-forming bacteria  The infectious process may spread into the thorax. and pulmonary infiltrates.Ludwig's Angina Page 135 of 217  An emergency and life threatening situation  generalized septic cellulitis of the submandibular region  occurs after dental extraction. drooling of saliva. other option is inhalation induction  Post-op keep intubated  to ICU until swelling subsided . and the difficult airway cart in the room. empyema C dehydration. pericardial effusion. CXR for Pneumothorax A difficult.  hemolytic streptococci. especially of the second or third mandibular molars  it’s bilateral. and the neck is prepped. aerobic and anaerobic. scrubbed. necrotizing fasciitis  Review the CT/MRI. pneumonia. and difficulty in speaking.

Lung volumes and capacities Page 136 of 217 .

Page 137 TABLE 30–7. Underestimation of Left Ventricular End-Diastolic Pressure of 217 CONDITION Decreased left ventricular compliance Aortic regurgitation Pulmonic regurgitation Right bundle branch block Decreased pulmonary vascular bed SITE OF DISCREPANCY Mean LAP<LVEDP LAP a wave<LVEDP PADP<LVEDP PADP<LVEDP PAWP<LVEDP CAUSE OF DISCREPANCY Increased end-diastolic a wave Mitral valve closure prior to enddiastole Bidirectional runoff for pulmonary artery flow Delayed pulmonic valve opening Obstruction of pulmonary blood flow .

 is associated with K.  protein-bound (30%). CHF. adenyl cyclase. and ionized (55%)  Magnesium is necessary for enzymatic reactions involving DNA and protein synthesis. phos.  The distal tubule of the kidney is the major site of magnesium regulation. proton pumps. and depression. confusion. Excessive Mg loss is associated with prolonged nasogastric suctioning. dysrhythmias. excessive Mg losses.  CV coronary artery spasm. and Ca. paresthesias. and intestinal drains . Ca-ATPase enzymes. most commonly caused by inadequate GI absorption.  S/S: weakness. GI or biliary fistulas. As a primary regulator or cofactor in many enzyme systems. 25% muscle.  Rarely resulting from inadequate dietary intake. and < 1% in the serum. chelated (15%). Hypomagnesemia  clinical features of Mg. and coma. 50% in bone.  can aggravate digoxin toxicity and CHF. magnesium is important for the regulation of the Na–K pump. lethargy. and hypotension. or failure of renal Mg conservation. Na. muscle spasms. like Ca neuronal irritability and tetany.Magnesium Page 138 of 217  mainly intracellular. When severe  seizures. and slow Ca channels.

excessive Mg losses.Magnesium Page 139 of 217  Mainly intracellular. coronary artery spasm. give Mg Hypermagnesemia  Most common cause is iatrogenic. lithium. or failure of renal Mg conservation. Excessive Mg loss is associated with prolonged NGT. diuretics. IV CaCl. gastrointestinal or biliary fistulas. M may associated with other electrolytes abnormality Rx stop NGT. CHF. other Addison’s disease. respiratory paralysis Cardiac arrest  Rx D/C Mg. dialysis . and intestinal drains. deep tendon areflexia Heart block. A N/A B N/A C arrhythmias. distal tubule is the major site of magnesium regulation Hypomagnesemia  Rarely from inadequate dietary intake. most commonly caused by inadequate GI absorption. BP. hypothy  S/S depend on Mg level  Hypotension Deep tendon hyporeflexia Somnolence Respiratory insufficiency.

need endocarditis prophylaxis Other lens dislocation.  length of long bone A TMJ laxity  dislocation with intubation B scoliosis. MVP. lytes. retinal detachment Position careful Neuraxial potential difficult. tamponade. may need a bigger dose and volume of LA Lab Echo. CBC. restrictive lung defect spontaneous Pneumothorax careful with PPV C cystic media necrosis. creat. CT-chest and angio all for dissection. MR. Pectus excavatum. valve. CXR pneumo. aortic dissection. AR. -blockers and volatiles are good. arrhythmia. kyphoscoliosis. BUN. aneurysm  Avoid sudden  in contractility. ABG.Marfan syndrome: Page 140 of 217  AD. PFT .

 If the anesthetic is discontinued. within 4–12 hours. anesthesia is induced by inhalation with halothane or sevo. (5) increased resting tension after succinylcholine in the presence of fever or elevated plasma epinephrine.Masseter Muscle Rigidity Page 141 of 217  most common in children and young adults. the initial signs of MH appear in 20 minutes or more. myoglobinuria occurs and CK elevation is detected.  Tachycardia and dysrhythmias are not infrequent.  DDx of MMR are: (1) myotonic syndrome. (4) not allowing sufficient time for Sux to act before intubation.  However. However.  Characteristically.  (if the anesthetic is continued with a triggering agent). peak age incidence at 8–12 yrs of age. after sucx is given.  A peripheral nerve stimulator usually reveals flaccid paralysis. . Snapping of the jaw or rigidity on opening of the jaw is seen. (3) underdosing with Sux.  Repeat doses of succinylcholine do not relieve the problem.  this rigidity can be overcome with effort and usually abates within 2–3 minutes. increased tone of other muscles also may be noted. the patient usually recovers uneventfully.  Muscle biopsy with caffeine–halothane contracture testing has shown that approx 50% of Pt who experience MMR are also susceptible to MH. (2) TMJ dysfunction.

Maxillofacial trauma Page 142 of 217  Lower 1/3  mandible (30% in the body of the mandible)  Middle 1/3  maxilla, zygomatic, orbital, nasal  LeForte I, II, III  Upper 1/3 frontal and cranium ( CNS) Airway  100% O2, and clear the A/W from foreign bodies, blood, # teeth (count), if there is bleeding apply pressure, nasal packing, and consider a close reduction for a #  In case of tongue injury  laceration edema/swelling  difficult intubation  In case of mid and upper facial injury avoid nasal intubation  Bleeding, and possible basal skull # Laryngeal injury  S/S hoarseness, stridor, sub-Q emphysema with crepitus  void blind technique  After intubation with direct vision bypass the injury and make sure that the cuff is beyond the injury Trismus after facial injury  due to muscle spasm  relived by GA

Meconium Aspiration: Page 143 of 217  Risk of PPHTN.   risk with post-term pregnancy  The new recommendation it does not matter thin or thick meconium  If there is meconium suction the hypopharynx  Apply NALS  If not vigorous (HR < 100, resp depression)  ETT suction, 100% O2  If vigorous  no need for ETT or tracheal suctioning

MH acute crisis Page 144 of 217 Manifestations :  Hypercarbia, Tachycardia, Tachypnea, Temp  (1°C–2°C increase every 5 minutes), HTN, Cardiac dysrhythmias, Acidosis, Arterial hypoxemia, Hyperkalemia, Skeletal muscle activity, Myoglobinuria  DDx: pheo, thyroid storm, carcinoid Management:  Call for help  Discontinue inhaled anesthetics and succinylcholine  Hyperventilate the lungs with 100% O2  Administer dantrolene (2.5 mg/kg iv) with repeated doses (up to a maximum of 10 mg/kg iv) based on Paco2, heart rate, and body temperature (each ampule of 20 mg is mixed with 50 ml of distilled water)  If Dantrolene is not available, give procainamide IV 1mg/kg up to 15mg/kg  Treat persistent acidosis with sodium bicarbonate (1–2 mEq/kg iv)  Control body temperature (gastric lavage, external ice packs until 38°C)  Replace anesthetic circuit and canister  Monitor with capnography and arterial blood gases  Be prepared to treat hyperkalemia and cardiac dysrhythmias

Mineralocorticoid Physiology Page 145 of 217  Aldosterone is a major regulator of extracellular volume and K homeostasis through the resorption of Na and the secretion of K.   Renal perfusion pressure+ sympathetic stimulation+ Na, and hypovolemia  renin from juxtaglomerular Renin splits angiotensinogen to angiotensin I ACE in the lung Angiotensin II aldosterone.  Other stimuli that aldosterone includeK and, to a limited degree, Na, PGE, and ACTH.  So  aldosterone  K and Na and HTN, while  is the opposite Mineralocorticoid Insufficiency:  Common in CRF, and DM, Pt usually on fludrocortisone 0.05-0.1 mg/d C hypovolemia, heart block due to K, M K, Na, and metabolic acidosis (hyperchloremic) D Avoid Sux, and NSAID   PGE  Renin  exacerbation

and approximately 25% have significant regurgitation. PAWP giant V wave. patients develop symptoms of fatigue and exertional dyspnea. Almost always associated with MS. or prosthetic valve dysfunction.  When CHF develops rapid deterioration with 5 yrs mortality rate 50% Physical Findings .  CTD associated with MR include SLE. infective endocarditis and LV hypertrophy. In acute MR there is sudden  in LAP pul edema. myxomatous degeneration(MVP).6 associated with severe MR. followed by more overt symptoms of CHF. Eccentric hypertrophy of the LV. Pathogenesis  Long latent period 30-40 yrs.  Valvular involvement in CTD is variable. LA volume overload LV volume overload with  foreword LV SV. including orthopnea and paroxysmal dyspnea. ank spondylitis.  Acute severe MR is caused by infective endocarditis which result in chordae tendineae.Mitral Regurgitation Page 146 of 217  Chronic regurgitation caused by abnormal leaflet anatomy can be due to congenital or rheumatic disease.  Later. acute MI with papillary muscle rupture or retraction usually from RCA. History  Patients with chronic MR remain asymptomatic for an extended period. CTD. rh arthritis. and scleroderma. Regurgitation fraction > 0. about 50% of patients with SLE have detectable MR.

5 cm . . fever.  Pul arteriolar and capillary vasoconstriction protect against pul edema. F>M.Mitral Stenosis Page 147 of 217  normal MVA 4. Pathogenesis  Obstruction to LV inflow  LA dilation and HTN and resultant pul venous HTN interstitial edema  work of breathing dysponea.5 cm2. 2 mild gradient < 5 mm Hg and VA >1. and predispose to supraventricular tachyarrythemia. emotional stress.  Pul HTN can be severe late in the course of MS. Symp(exercise or tachycardia) 2.  The MV is the most common site of rheumatic valve disease. rest < 1. including strenuous physical exercise.0 to 6.g. Long latent period > 20 yrs.0 cm2.5 cm2. PE which can lead to pul edema  Stasis of the blood in the LA thrombi A fib systemic emboli. pregnancy. History  Early fatigue or dyspnea precipitated by events with associated tachycardia. or surgery.  Acute decompensation occur due to stress e. A fib. Severe gradient > 10 mmHg. pregnancy.0 to 2. with eventual RV systolic dysfunction. MS in adults is predominantly of rheumatic origin. although  PVR exacerbates pul arterial and RV HTN and causes RVH. and valve area < 1 cm2. sepsis.

but if severe then art-line. aggressively treat arrhythmia o Cont  maintain. LUD. CVP/PAC  MVP manage as MR .fib with systemic embolization due to hypercoaglable state in pregnancy  hemodynamic Goals: o preload maintain.MR Page 148 of 217  Well tolerated in pregnancy   risk of A. avoid overload o R/R  slightly  maintain sinus.  PCO2  If mild no need for aggressive monitoring. hypoxia. avoid cardiodepressant o Afterlaod  o PVR avoid pain.

O2 all the time  In the 2nd stage avoid explosive effort  valsalva  VR pul edema  Avoid overzealous hydration  pul edema  Tachycardia  -blockers  hemodynamic Goals: o preload maintain.  Arrhythmias are not tolerated at all. hypoxia. Digoxin.MS Page 149 of 217  Not well tolerated. PAC. LUD. and needs to treated very aggressively with -blockers. over even cardioversion. then lasix   mortality during labor/post-partum  Mild is usually tolerated ok  But mod/severe  pregnancy worsen NYHA by 1-2 classes  Need invasive hemodynamic monitoring art-line. avoid overhydration o R/R  slow and sinus o Cont  maintain. avoid sudden  in SVR o PVR avoid  by pain. avoid cardiodepressant o Afterlaod maintain. PCO2  Neo is the best choice in case of hypotension . with  risk of pul edema.

short neck  difficult A/W B Restrictive defect C CAD. VHD. AO instability. Cardiomyopathy GI hepatosplenomegaly MSK joint stiffness. macrogolssia. CXR . kyphoscoliosis. odontoid hypoplasia.Mucopolysaccharoidosis: I H Hurler I H/S Hurler/Scheie I S Scheie II Hunter III Sanfilippo IV Morquio Page 150 of 217 A Coarse facial features. Dwarfism  Routine lab + Echo. AR.

Multiple Sclerosis Page 151 of 217  demyelination in the brain and spinal cord, F>M  symptoms depend on the sites: visual disturbances, nystagmus, limb weakness and paresthesias, The legs are affected more than the arms.  Bowel retention and urinary incontinence are frequent complaints.  Involvement of the brain stem can produce diplopia, trigeminal neuralgia, cardiac dysrhythmias, and autonomic dysfunction, while alterations in ventilation can lead to hypoxemia, apnea, and respiratory failure.  As is typical in many immune disorders, pregnancy is associated with an improvement in symptoms, but relapse frequently occurs in the first three postpartum months.  treatment Corticosteroids, immunosuppressants (azathioprine, methotrexate, cyclophosphamide, and cyclosporine)  Symptoms exacerbation with stress (emotional, surgical)  temp, infections Management of Anesthesia  Possible exacerbation post-op  Document neurological symptoms pre-op, re-exam post-op  the patient should be advised that surgery and anesthesia could produce a relapse despite a well managed anesthetic

Murmurs Page 152 of 217  Innocent murmurs: soft, systolic and not radiated, may vary with position, not characteristic of any lesions  Noninnocent murmurs: all diastolic murmurs, all pansystolic, continues, late systolic and transmitted murmurs  For innocent murmurs no need for surgical delay, and no need for prophylaxis  Not noninnocent one’s if heard in the pre-op delay, and further investigation

Midsystolic Page 153 of 217  flow across aortic or pulmonic valve (e.g., secondary to AR or ASD) Aortic valve leaflet sclerosis (e.g., in elderly patients) Aortic or pulmonic outflow obstruction (valvular, subvalvular, supravalvular) Dilatation of aortic root or proximal pulmonary artery Papillary muscle dysfunction Holosystolic MR, TR, VSD Late Systolic MVP, Papillary muscle dysfunction Early Diastolic Aortic or pulmonic valve insufficiency Mid-Diastolic MS, TS  flow across nonstenotic AV valve (e.g., secondary to MR or ASD) Presystolic MS (with sinus rhythm) Continuous Murmurs PDA

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Muscular dystrophy

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7 main types with progressive and variable rate in losing of muscle function. The most common, and the most severe form. Due to lack of protein Dystrophin. Painless degeneration of the skeletal muscle. X-linked trait (boys) S/S 2-5 yrs old. In the wheelchair by age of 12. The affected muscle may become enlarged, due to fatty infiltration. Death by 15-25. Secondary to CHF and pneumonia. Serum CK reflect the progression of the disease, with 30-300 folds above normal, later with complete degeneration the level well . Smooth muscle involvement  GI hypomotility and gastroparesis. CVS o myocardial degeneration loss of R-wave in the lateral leads o  contractility dilated cardiomyopathy, and arrhythmias

Duchenne’s muscular dystrophy

if MR  late systolic murmur A N/A unless associated with other disease B if CHF  plu edema. anticoagulants  P/E  late systolic click.  Risk of endocarditis. Endocarditis prophylaxis D avoid histamine releasing drugs. anxious Pt may benefit from pre-op meds Hemodynamic goals Preload maintain Contractility avoid  R & R  sinus. stroke.g. Diuretics. sudden death  If associated with MR or CHF. little fast Afterload avoid . connective tissue disease. antiarrhythmics. Pt could be on ACEI. marfan syndrome. Arrhythmias. arrhythmias. -blockers. better  . ? scoliosis  restrictive lung defect C CHF.MVP: Page 155 of 217  More common in young female than in male  May associated with other disease e. and ketamine CNS Stroke.

 underdosage  ―myasthenic crisis‖ whereas overdosage will produce a ―cholinergic crisis. 75% of pts either go into remission or are improved post-op  Medical ttt: anticholinesterase. bradycardia. diarrhea. cyclosporine)and plasmapheresis.‖ Excessive doses of cholinesterase inhibitors produce abdominal cramping.Myasthenia Gravis Page 156 of 217 Osserman and Genkins classification: • Class I—ocular symptoms only • Class IA—ocular S’s with EMG evidence of peripheral muscle involvement • Class IIA—mild generalized symptoms • Class IIB—more severe and rapidly progressive symptoms • Class III—acute. to differentiate . other immunosuppressant (azathioprine. 15% thymoma). vomiting. salivation. cyclophosphamide. steroids. F>M  Abnormal thymus glands 75% of pts(85% show hyperplasia. and skeletal muscle weakness that mimics the weakness of myasthenia . presenting in weeks to months with severe bulbar symptoms • Class IV—late in the course of the disease with severe bulbar symptoms and marked generalized weakness  autoimmune disease with anti-acetylcholine receptor antibodies.

Pt could be on diaminopyridine  Sz  Keep high index of suspicion in a Pt with Lung Ca  Consider Art-line . age 50-70  Mainly proximal muscle weakness A B rarely respiratory failure C autonomic dysfunction  orthostatic hypotension D sensitive to both Sux and NDMR.Myasthenic Syndrome (Lambert-Eaton Syndrome) Page 157 of 217  Associated with small cell ca of the lung  IgG antibodies against Ca channel in the presynaptic membrane   Ach release in response to nerve stimulator  M>F.

Page 158 of 217 .

NALS Page 159 of 217  Exam table goes trend for drainage and reverse trend to  PO2  Avoid hypothermia   VO2  metabolic acidosis  Assess for choanal atersia  usually cyanotic and resp depression at rest. dry. give O2  not breathing or HR < 100 PPV with initial P 30-40 cmH2O for 4-5 sec to open the alveoli..5 sec  90:30 pre minute  Chest compression using two thumbs just below a line drown between two nipples to compress the AP diameter by 1/3 to ½  Intubation can be considered at any time  If Vent without ETT for > 2-3 min  decompress the stomach . and Pink ongoing care. the vent @ rate 40-60 min  if HR > 100.5:0. tactile stimulation by rubbing the back.  For vent I:E = 1:1.. flicking the soles of the foot. pink when crying  If Apgar score < 8 with not resp depression give O2 by ―blow by‖  So If not breathing or cyanotic suction the A/W. Bicarb………. after the 1st breath the P 20-30 cm H2O  For chest compression to vent 3:1  1. @ 40-60 min. warmth. if HR < 60 PPV and start Chest compression for 30 sec  if still HR < 60 five Epi  ….

pul edema C septic shock with  SVR. malnutrition. respiratory failure.  CO M lactic acidosis. alcoholism. possible under resuscitated A full stomach  RSI B ARDS. renal and CV diseases  Septic shock. lytes abnormalities R ARF CNS   LOC  Lab and Mx as septic shock  Post-op  ICU .Necrotizing fasciitis Page 160 of 217  Emergency and life threatening with high mortality rate  Possible underlying disease: DM.

immature renal function CNS fragile cerebral vessels  risk of IVH  by hypoxia. glucosuria H2O and lytes depletion Physiological jaundice  alter drugs pharmacokinetics. hypercarbia. fluctuation in BP. convulsion Glucose infusion @ 4-8 mg/kg/min  hyperglycemia  cerebral hemorrhage. hypothermia Renal  Na loss. acidosis. Na. low Hb. and  free bili kernicterus.Neonatal Considerations: Page 161 of 217 In addition to the pediatrics considerations Metabolic risk of hypoglycemia S/S: apnea. which  by hypoxia. rapid administration od NHCO3 Eye ROP maintain O2 sat 90-95% or PO2 50-70 .

smoking. position  A block done or not if yes any symptom at the time of the block pain or paresthesias with injection  If the surgical procedure done in the same side  ? surgical complication or prolonged use of a tourniquet. motor  further evaluation . and mainly examining the affected side sensory.Peri-op nerve injury: Page 162 of 217 History:  Symptoms: pain. complete neurological exam. motor weakness. motor. also BP cuff may cause injury Exam:  V/S. when did it start  Presence of risk factors or conditions that may have neuropathy as a symptoms: DM.  Drugs that may cause neuropathies  chemo. and looking for any pressure demarcation  Also assess for nerve or dermatomal distribution Obtain a Neurology consult for further evaluation and need for nerve conduction study. paresthesia. Obesity. OR note for documentation of padding. and possible MRI  Sensory only F/U in 2wks. alcohol. PVD. reflex. anti-virals  Review anesthetic records. R Arthritis. where.

Neuraxial Anesthesia and anticoagulation Page 163 of 217  IV heparin e.4 is OK . if Pt receiving a higher dose 1mg/kg  delay 24hr  Post-op 1st dose of LMWH delay 24 hr. or delay the heparin 1 hr post catheter placement  LMWH: needle placement 10-12hrs after the last dose of LMWH.C heparin also delay catheter placement 2-4 hrs. and catheter removal 2-4 hr after the last dose or one hr before the next dose  S. vascular Sx  delay IV heparin 1hr post catheter placement.g. but better at least 10 days before needle placement. give LMWH 2hrs later  Anti-PLT: plavix ?? no data. NSAID are OK  Pt on oral med (Warfarin)  stop 5 days per-op INR= 1. and may keep the catheter until next AM.

Echo. creat. Avoid if there is spinal cord tumor  Lab CBC.Neurofibromatosis Page 164 of 217  AD. with > 1. BUN. meningioma (ICP). possible mediastinal mass C HTN due to renovascular. coarctation.5 in diameter. CXR. ECG. interstitial lung disease. Pheo. Wilm’s tumor CNS Astrocytoma. PFT with F/V loop . and short stature  Could be a part of MEN IIB A difficult intubation. spinal cord tumor. Sz disorder M diffuse endocrine disorder as well as carcinoid tumor MSK  Kyphoscoliosis  Regional Anesthesia  could be difficult. with CNS vascular and skin involvement. Lytes. café-au-lait spots >6. due to laryngeal or tracheal compression B restrictive lung defect.

is often useful in treatment of NMS   with dehydration.  Phenothiazines and haloperidol or any of the newer potent antipsychotic agents alone or in combination are usually triggering agents for NMS  Sudden withdrawal of drugs used for Parkinson's disease may also trigger NMS  (ECT) with Sux does not appear to trigger the syndrome. a dopamine agonist. whereas NMS often occurs after longer term drug exposure. hypertension. . . agitation. and myoglobinuria  The mortality rate is unknown. rapid titration of triggering drugs. MH is acute. rhabdomyolysis. and psychomotor agitation  Other DDx: CNS diseases  meningitis.  there are significant differences between the two.  possible due to dopamine depletion in the CNS by psychoactive agents. tumor. Dantrolene is an effective therapeutic modality in many cases of NMS.  bromocriptine. tachycardia. mental changes. hypoxia. muscle rigidity. acidosis. CK.  does not seem to be inherited. and acidosis. but may be as high as 20%.Neuroleptic Malignant Syndrome (NMS) Page 165 of 217  S/S include fever. and stupor.

Opioids. acid-base status.Non-obstetrical surgery during pregnancy Page 166 of 217  Obstetric consideration   Risk of abortion and premature labor  Minimize the amount of drugs as much as possible  Use only the drugs that are known to be safe(STP. and post op. Sux. and do RSI. with maintaining LUD . Oxygenation. for >16 wks have it intra-op for abdominal procedure consider a transvagainal monitor  FHR variability present @25-27 wks  Maintain normal maternal BP. Etomidate)  If urgent Sx consider delay to the 2nd trimester  Have an obstetric consultation  For GA < 16 wks have FHM pre. Ketamine. avoid aortocaval compression  For pelvic and lower limb and upper limb consider regional technique  For laparoscopic procedures max peritoneal inflation pressure 8-12 mm Hg  For spinal or epidural give a fluid bolus before  Always give reflux prophylaxis. NDMR.

EXAM RV/LV failure  LAB CBC-D. BUN. PND.Obesity Page 167 of 217 A difficult intubation B OSA. and regional anesthesia .  gastric acidity. ABG. PFT.LFT. and consider Echo  Difficult IV access. Lytes. and RV/LV dysfunction  snoring. pickwickian syndrome. CAD. restrictive defect. orhtopnea. with  FRC and Pul HTN C HTN. Creat. pul HTN with cor-pulmonale. fatty liver with liver dysfunction M DM D calculate the drug dosage according to the lean body mass  H/P evidence of OSA. RV and LV dysfunction GI GERD. ECG.

 gastric empting. Full stomach.Obstetric considerations: Page 168 of 217  Physiological and anatomical changes A difficult A/W.  cholinesterase. .  albumin  Free F of drugs.  UP blood flow D   MAC.  VO2 C hyperdynamic state. Aortocaval compression   BP.RSI B easy desat   FRC.  liver enzyme . placental drug transfer GI/Hepatic  full stomach.

a large tongue. with lytes abnormality . and an omphalocele.Omphalocele and Gastroschisis Page 169 of 217 o Impaired blood supply to the herniated organs. and intestinal obstruction o Major intravascular fluid shift and dehydration full-strength balanced salt solution o Hypothermia and hypoglycemia A possible difficult airway  Beckwith-Wiedemann syndrome consists of mental retardation. and arterial line Post-op keep intubated M  intravascular volume. congenital heart disease. B respiratory failure C CHD in 20% of infants with omphalocele. hypoglycemia. possible central. need large IV . Induction: NG  aspirate gastric content then RSI .

. aspiration B Respiratory failure. diarrhea U urination M miosis B bradycardia. QT(poor prognosis) D Avoid aminoglycosids ABx M lytes abnormalities. bronchospasm C hypotension. dehydration GI N&V. shock. bronchorrhea. bronchospasm E Emisis L lacremation S salivation A salivation. arrhythmias.Organophosphate poisoning  Bind to acetylcholinestrase enzyme  S/S: Nicotinic: muscle weakness. bronchorrhea. bradycardia. fasciculation Muscarinic: DUMBELS syndrome D diaphoresis. acidosis. diarrhea Page 170 of 217 .

vertebral # Awake FOI B kyphoscoliosis  restrictive lung defect C Cor-pulmonale Heme impaired PLT function Page 171 of 217 . short stature. blue sclera A deformity of the base of the skull.Osteogenesis Imperfecta:  A connective tissue disorder with 4 subtypes  Multiple #.

Other hemolytic anemia’s: Page 172 of 217 Spherocytosis:  Membrane defect  abnormal shape RBC hemolysis  May have a hemolytic crisis which can triggered by infection and folate deficiency  May come for splenectomy G6PD Deficiency:  RBC enzyme defect  Can have a hemolytic crisis if exposed to some food and drugs: Fava beans. antimalarial drugs. methylene blue. ASA in large dose  Usually happened 2-5 day after ingestion  May have DIC . Tyhlenol. PNC.

 Oxygen delivery is a function of arterial oxygen content (Cao2) and cardiac output.34 × Sao2) + (0.Oxygen Delivery and Oxygen Consumption Page 173 of 217 Oxygen Delivery.003 × Pao2) DO2 = CO × Cao2 Oxygen Consumption. Cao2 is expressed as the number of milliliters of oxygen contained in 100 ml of blood and is calculated as follows: Cao2 = (Hgb × 1.  O2 consumption = CO x (CaO2-CvO2) Oxygen extraction Ratio ER= O2 consumption / O2 delivery ER= [ CO x (CaO2-CvO2)] / CO x CaO2 = CaO2 – CvO2/CaO2 .

old blunt trauma A RSI. for GI ileus B ARDS C  hypovolemia. CF. chronic) Page 174 of 217  Associated with: chronic alcohol abuse. CVP  Post-op ICU. acidosis. pain management . DM. gallstone. blunt abdominal trauma.Pancreatitis:( acute. hypotension D narcotic tolerant. Pneumonia  Chronic mainly with alcoholism. malnourished   albumin   free fraction of drugs  careful titration M   Ca. perforated PUD  Lab   amylase  DDx  cholecystitis . MI. acute alcohol withdrawal Renal ARF  due to dehydration CNS encephalopathy Heme anemia. DIC  Consider art-line .

Demerol. avoid Maxran. . COPD C arrhythmias due to L-dopa. droperidol. bradykinesia.Parkinson's Disease Page 175 of 217  degenerative disease of the CNS caused by loss of dopaminergic fibers in the basal ganglia of the brain. stooped posture. alfenta. K one case report Post-op: In the postoperative period. and facial immobility.  VC.(substantia nigra)  clinical features are resting tremor. cogwheel rigidity of the extremities. sux may use for RSI. muscle rigidity before giving MR difficult vent consider RSI B frequent aspiration. patients with Parkinson's disease are more susceptible to the development of mental confusion and even hallucinations. A laryngospasm.  intravascular volume D L-dopa(sinemet) Levodopa+ a peripheral dopamine decarboxylase inhibitor carbidopa to  systemic side effect give in AM t1/2 6-12. autonomic dysfunction. shuffling gait.

Tylenol. caffeine 300mg PO q8-12hrs. type and size of needle for spinal. and any other complications  Review past-medical Hx neurological Hx (headache)  Headache: character. associated symptoms. photophobia. and wet tab documentation. severity. tinnitus. migraine Action:  Review anesthetic Record for Neuraxial procedure. sitting  severe fronto-occipital headache  May associated with cranial N symptoms: diplopia. fever). hydration. gentle intubation avoid rupture the abscess .PDPH Page 176 of 217  In a supine position very mild. aggravating and relieving factors (position). N&V  DDx: meningitis. Neuro Exam looking for any sensory or motor deficit  Rx: bed rest. do a gas induction with no muscle relaxant . and NSAID’s if not working or severe headache  Epidural blood patch Peri-tonsilar abscess Emergency and potential life threatening A airway obstruction. possible full stomach. meningeal signs (meningismus. and the location of the headache  Exam: V/S include Temp. with trismus .

. pheochromocytoma.Pheochromocytoma Page 177 of 217  In normal medulla.  extra-adrenal sites (10%) along the paravertebral sympathetic chain.  halothane and histamine-releasing drugs. urinary bladder. 10% of adults and 25% of children have bilateral tumors.  Malignant spread of highly vascular tumors in approximately 10% of cases. or neck. a small % located in thorax. norepinephrine account for only 20% of the secretion.  may also arise in association with von Recklinghausen's neurofibromatosis  or von Hippel-Lindau disease (retinal and cerebellar angiomatosis). this tumor is inherited as a familial AD trait. pheochromocytoma. where it is greater in a Pt with pheochromocytoma. can exacerbate the life-threatening cardiovascular effects of the catecholamines secreted by these tumors. parathyroid hyperplasia. neuromas of the oral mucosa.  95% in the abdomen.  Type IIB consists of: medullary carcinoma of the thyroid.  Type IIA includes: medullary carcinoma of the thyroid.  In about 5% of cases.  It may be part of the polyglandular syndrome as MEN Type IIA or IIB.  usually the right.  Most (85–90%) are solitary tumors localized to a single adrenal gland.

 As part of 2.Phosphate Page 178 of 217  distributed in similar concentrations throughout intracellular and extracellular fluid. in the ECF. and <1%.  Phos is an essential element of second-messenger systems.  Phos provide the primary energy bond in ATP and creatine phosphate.3-DPG. phospholipids. 10% is intracellular. severe phosphate depletion results in cellular energy depletion. and a major component of nucleic acids. phos is important for off-loading oxygen from the hemoglobin molecule. and insulin-like growth factor. dietary intake. complexed ion (33%).90% in bone. including cAMP and phosphoinositides. Phos reabsorption in the kidney is primarily regulated by PTH. and in a protein-bound form (12%). and cell membranes. . Therefore.  Absorption occurs in the duodenum and jejunum and is largely unregulated.  Control of phos concentration by altered renal excretion and redistribution within the body compartments.  free ion (55%).

URTI and fluid overload. edema. TV. easy nasal bleed B FRC.  IRV.  by PIH. cleft palate B obstruction pul edema. and O2 consumption. have ENT surgeon in the room for possible trach  A/W obstruction improve with age  Extubate awake only . shift of O2-Hgb curve to the Rt with P50 30mmHg C  CO. Aspiration C CHF.Physiological changes in pregnancy: Page 179 of 217 A venous engorgement. TLC. cor pulmonale. pul HTN. Normal BP due  SVR. associated CHD CNS Sz due to hypoxic brain injury  Do awake FOI. glossoptosis.  shunt from 5% to 14 %. minute vent. ERV.  plasma volume Pierre Robin Syndrome: A difficult A/W due to micrognathia.

PT. other meds. BUN. blurred vision.  BP.  fibrinogen CNS  LOC.  oncotic pressure D Mg. consider other anti-HTN meds e. Mg. (ACEI are C/I due to fetal effect)  Monitor Mg level avoid Mg toxicity. improve UP blood flow (if PLT are OK)  Monitors: art line. fibrinogen. seizure. Lytes. thrombocytopenia . could be on ASA M  Mg. consider early epidural  help  BP. labetolol. SNP.g. ARF GI/Hepatic  RUQ pain.  volume. difficult intubation difficult A/W cart in the room B pul edema. Creat. more after delivery C CHF. fetal monitoring. hydralazine. LFT. liver rupture  Rx start Mg bolus 4g then infusion @ 1-3 g/h. hemolysis. headache.PIH and HELLP Page 180 of 217  In addition to the changes in pregnancy A  airway edema. BT . PTT. CVP/PAC  Before giving any fluid bolus look for evidence of CHF  Lab: CBC-D.  albumin Heme anemia. bleeding . NTG. edema Renal  GFR. oliguria.

or pan-hypopitutarism  hyper secreting could be a MEN I. or hyper secreting  The non-functional  mass effect  headache impaired vision. IV. then GH. and transsphenoidal approach Page 181 of 217  Ant regulated by the hypothalamus secret 7 hormones  Post ADH. cardiomyopathy D hormone replacement. stress dose steroid. then ACTH. lytes. usually small.Pituitary Tumors. Oxytocin  Tumors could be non-functioning. and  ICP. V. Cardiomegaly. ECG. . lateral neck XR  Critical structures internal carotid artery. ABG. the most common is adenoma secreting prolactin . CXR. DM  pituitary apoplexy  due to sudden hemorrhage  neuro deficit and  pituitary function  Mx  steroids and surgical decompression  May not develop DI until after starting steroids therapy  Monitors routine with art-line for acromegaly. cavernous sinuses. CVP if head-op position  Lab  CBC. VI A possible difficult intubation B OSA C HTN. CN palsy. N&V. other effect hyperthyroid. CN III.

most are dilutional thrombocytopenia Mx: lab as in abruption shock as in abruption GA Vs spinal/epidural depend wither if the placenta is anterior or >1 C/S with  risk of accreta  GA. if posterior may consider spinal/epidural if the Pt is stable .Placenta previa Page 182 of 217  Risks: previous C/S. previa  Painless vaginal bleeding in the 2nd-3rd trimester  Risk of abruption and IUGR  Avoid vaginal exam and tocolytic therapy A and B  obst C hypovolemia. shock D avoid tocolytic Heme DIC rare.

Porphyrias Page 183 of 217  A group of inborn error of metabolism. which are:  Acute intermittent Porphyria  variegate Porphyria ( 80% photosensitive)  hereditary coproporphyria o noninducible forms. . with defect in heme synthesis  Complete deficiency of enzymes is incompatible with life  Deficiency of one enzyme will lead to accumulation of one or more intermediates molecules which will give the clinical manifestation of Porphyria. Inheritance is an AD pattern.  generally manifest after puberty.  The rate-limiting step in heme synthesis is the conjugation of succinyl-CoA with glycine to form D-aminolevulinic acid ALA (the enzyme is aminolevulinic acid synthetase).  but congenital erythropoietic porphyria is inherited as an AR pattern.  A functional classification for the anesthesiologist is based on a division of the porphyrias into: o Inducible: acute symptoms are precipitated on drug exposure.

blood.Post-op Stridor: Page 184 of 217  Emergency. vomit . and life threatening  Proceed immediately to the PARR  Review the V/S. 100% O2. 2-laryngeal edema due to volume overload or Trendelenburg position intra-op.3. suction the A/W  DDx: 1-Laryngeospasm.VC paralysis due to neck or thoracic Sx. or residual NM blockade. and quick AMPLE history .A/W foreign body (secretion. 4. do jaw thrust. and Call for help. apply oral A/W. apply CPAP.

CVA. Ketamine. obtain new V/S  Review anesthetic chart/ talk to the anesthetist who did the case. seizure.Post-op Altered LOC/Agitation: Page 185 of 217  With  LOC could be life threatening. review the old chart  DDx: o Psychological response to emergence o Co-existing mental/psychological problem (post-traumatic stress) o Intra-op re-call o Residual anesthetics. Ca. restrain the Pt if needed. agitation potential harm to him self and nurses  Proceed immediately to the PARR  ABC. postictal . Sz. o Drugs/alcohol withdrawal o Withdrawal of anti-psychotic. 100% O2. Parkinson meds o Surgical pain. hypoglycemia o CNS: hypoperfusion. NMB Agents. bladder distention o A/W obstruction  with hypoxia and hypercarbia o Other metabolic abnormalities  Na.

hypotension. hypovent.  retics 6) Review anesthetic and PARR records for any evidence of hypoxemia. and ALP  Most likely multifactorial  One of the main factors could be intra-op hepatic hypoxemia  Steps: 1) Review all meds given to the Pt without any exclusion peri-op. PE. resp failure. intra and post hepatic  The main S/S is jaundice  Need repeat measurement of bili.Post-op hepatic dysfunction Page 186 of 217  Classify as pre. hypovolemia 7) Look for extra-hepatic source of liver dysfunction CHF. includes intra-op use of vasopressors  splanchnic vasoconstriction  B flow 2) Look for source of infection 3) Blood Tx bili load  in Pt with co-existing liver dysfunction 4) Look for hematoma hyperbilirubinemia 5) Role out hemolysis  Hb. AST/ALT. RF 8) Could be benign post-op intrahepatic cholestasis .

possible difficult airway use ketamine for induction. RSI B  hypoxia C hemorrhagic shock. PTT. PT. X-match . resuscitate the Pt H possible bleeding disorder.Post-tonsillectomy bleeding Page 187 of 217 Emergency and potential life threatening Go immediately to see the Pt OR emerg meds . airway equipment double setup X2 suction . Lab CBC. lytes. X2 scops A  full stomach.

with balloon dilation only. wait only for one week for elective procedure.Pre-op Cardiac evaluation: Page 188 of 217  See other card for clinical predictors  See other card for stratification for noncardiac surgical procedure  See the algorithm  Recent MI wait 4-6 wks for elective surgery  Lab evaluation o Resting LV function is not a predictor for ischemic event o 12 leads ECG o Exercise or pharma stress test for Pt with intermediate risk. or when Pt is unreliable o Angio for Pt suspected or known CAD  Pre-op therapy o CABG for high risk Pt. for anti-PLT therapy o Medical: -blokers  Anesthetic consideration o No technique is superior . with possibility to improve outcome o PCA: no controlled trial for PCA vs medical therapy. if stent 4-6 wks with minimum 2 wks. If Pt had PCA.

and hyperventilation  K o Lidocaine IV may prevent arrhythmia  MgSO4 o See PIH for S/E. less severe than -agonist o Risk of hypotension with spinal/epidural o  sensitivity to NDMR . hypotension. tachycardia. need at least 10 min D/C before giving anesthetic o S/E: hyperglycemia. cerebral vasospasm. fetal tachycardia. pul edema. with possible arrhythmia. myocardial ischemia. rebound hypoglycemia o Avoid overzealous hydration which may  risk of pul edema.Preterm labor Page 189 of 217  Between 20-37 wks   fetal M&M  Pt may given tocolytic therapy if there is no C/I  -agonist: Ritodrine and terbutaline o For short term only to allow time for lung maturity after steroids o The effect persist to 60-90 min after D/C.

toes. CVP. SV. breast.  Venus return  due to pressure on the abdomen vena caval pressure  epidural vein engorgement .Prone position Page 190 of 217  Difficult access to the A/W  Difficult resuscitation  Difficult to add invasive monitoring art-line. iliac crest. genitalia  Brachial plexus injury   CI. TEE  Pressure injury to eyes. knees. nose.

and DIC. Antithrombin III deficiency   risk of thrombo-embolic phenomena  Resistance to heparin. or Acquired due to hepatic dysfunction. with possible Pul HTN.Protein C and Protein S Deficiency Page 191 of 217  Congenital  AD. C IHD (MI. TIA’s  for neuraxial anesthesia look in the ASRA guidelines  may give FFP to  protein C level. angina). CNS sagital sinus thrombosis  stroke. or FFP . vit K deficiency. hemodialysis. postpartum   risk of thrombo-embolic phenomena post-op A N/A B  PE. post-op. Peripheral vascular disease D on coumadin  stop pre-op and start heparin G bowel ischemia R renal vein and artery thrombosis. may give Antithrombin III concentrate.

CCB.  Consider: NO. avoid cardiodepressant o Afterlaod maintain. avoid sudden  in SVR o PVR  Avoid any thing that  PVR  pain. PCO2  O2 all the time. Art-line. acidosis. LUD o R/R  maintain normal and sinus o Cont  maintain. NTG to  PVR  PAC  risk/benefit  No spinal. epidural slowly titrate  GA same problem as in Eisenmenger  Post-op ICU . prostacycline.Pul HTN Page 192 of 217  The pulmonary vessels are more reactive compared to Eisenmenger  High mortality rate  Hemodynamic Goals: o preload maintain. hypoxia.

Pulmonary embolism Page 193 of 217  Associated with hyper-coagulation state (protein C and S deficiency ). V/Q scan. hypercarbia o  PVR. trauma. and PLT count (HIT)  Better to avoid Neuraxial technique in those Pt  If diagnosis is in doubt  Spiral CT. prolonged bed rest  High M&M  Pathophysiology: o Pulmonary arteries obstruction   dead space ventilation  hypoxemia . and now anticoagulated  have a hematology consult (Q: risk/benefit of holding meds pre-op) also discuss with the surgeon regarding continuing the anticoagulation med periop  Have PT. Bronchospasm o RV dysfunction and arrhythmias  Pt may present to the OR for emergency surgery. insertion of IVC filter or surgical embolectomy  Also Pt may present with previous history of PE. Echo . PTT.

cystic fibrosis. restrictive lung disease. ECG look for acute strain pattern in leads II. COPD. graham steel murmur  Lab: CXR. easy fatigue wheezing. sickle cell  S/S  SOBOE. o heart disease: MS. ABG. ASD. VSD o collagen vascular disease o thromboembolic disease: PE. AS. hypothermia. TEE. art-line.  PCO2) . Echo. NO test to if responsive or not (Viagra)  Cardiology consult and ICU  Monitors: CAS. and inotropic support (milrinon. 5 leads EGC. with exercise > 30  Primary (idiopathic) F:M 3:1. CVP. dobutamine) SNP. ECG(RVH. PAC???.Pulmonary HTN Page 194 of 217  @ rest mean of 25. age 20-40  Secondary: o pul disease: asthma. RAD. better RA  Have NO ready. PFT. NTG  Keep 100 O2 all time  Avoid things  PVR ( hypoxia. acidosis. Rt atrial enlargement). III and aVF  Options RA Vs GA.

anterior fontanel.2. V/S  Check lytes Na >132. insert NGT. or OGT to empty the stomach (no guaranteed) and pre-oxygenate  RSI with cricoid pressure  Maintenance  need to be paralyzed  if not risk of mucosal perforation  Infiltrate Marcaine with epi. moist tongue. S/S appear 2-6wks  With the consideration of neonate A full stomach RSI B compensated resp acidosis  hypoventilation C hypovolemia  shock M hypochloremic metabolic alkalosis. Cl>88. dehydration  Pre op assess the level hydration skin turgor. if + urine OP  Induction give atropine.  Give K. urine OP. K > 3.Pyloric stenosis Page 195 of 217  M>F  Not a surgical emergency. give Tylenol 15mg/kg PR for pain control .

Hemochromatosis. Radiation o Infectious: viral myocarditis o Infiltration: endomyocardial fibrosis o Genetic o Idiopathic o Infiltration  Sarcoid.Glycogen storage disease  Impaired diastolic filling  Have the same clinical picture of constrictive pericarditis  Except that the LV is more affected than RV  Management of anesthesia: o As Tamponade . Amyloidosis .Restrictive Cardiomyopathy Page 196 of 217  Causes: o Toxic :Methysergide. Anorectic agents.

where the acute component could be reversible  Causes: o intrinsic lung disease ( edema. aspiration. or idiopathic. and plural diseases) o Neuromuscular diseases: spinal cord transection. Guillian barre. and myasthenic syndrome o MSK scoliosis. BUN. Echo . lytes. with S/S of Rt heart failure  Pre-op: determine the severity by H/P and Lab. normal FEV1/FVC. and possible hyperventilation with  PCO2  Could be acute Vs chronic. RR  With severe disease Pt may have pul HTN. ARDS. and  VC  N 70ml/kg. myasthenia.  exercise tolerance. ECG. ascites  S/S SOBOE. muscular dystrophy.Restrictive lung disease Page 197 of 217  The main feature is  lung compliance with  TLC. sternal deformity o Extrinsic: obesity. breathing pattern Vt. CXR. fibrosis due to drugs. pregnancy. ABG. PFT. cough.  as low as 15ml/kg. creat. and treat the possible acute reversible component  A VC < 15ml/kg with  PCO2  high risk  Lab: CBC-D. pneumonia.

pulmonary nodules.  B: pleural effusions. and risk of postextubation stridor. TMJ involvement. obstructive lung disease. particularly the metacarpophalangeal and proximal interphalangeal joints. coronary arteritis  dysrhythmias secondary to development of rheumatoid nodules in the cardiac conduction system  aortitis. Cricoarytenoid arthritis which may cause pain. Valve fibrosis . restrictive lung disease.. interstitial lung disease. horseness. producing aortic root dilation and aortic insufficiency.  A:C-spine: atlantoaxial subluxation. and asymptomatic patients may have a high degree of spinal canal stenosis. more common due to costochondral involvement  Several of the antirheumatic drugs cause pulmonary dysfunction as well  V/Q mismatch and hypoxia Consider PFT and possible post-op ICU bed  C: Pericarditis in 30%. So be caution with intubation and consider Fiberoptic intubation. dyspnea.Rheumatoid arthritis Page 198 of 217  F> M. chronic constrictive pericarditis or pericardial tamponade myocarditis. The degree of cord compression does not correlate well with the patient's symptoms. Age 30-50  The hands and wrists are involved first. stridor and airway edema.

o Signs hypotension. and hypothermia o ECG  peaked T waves. and flattened T waves. o If ECG changes are observed the transfusion should be stopped and intravenous calcium should be administered. o Citrate is metabolized efficiently by the liver. and insulin may also be appropriate according to the severity of the episode  Volume Overload  Hypothermia   CO. widened QRS. Bicarbonate.3-DPG left shift of the O2–Hgb dissociation curve  Hyperkalemia with rapid Tx   by acidosis.Risk of RBC Tx Page 199 of 217  Citrate Intoxication o CPDA citrateionized calcium. left shift of O2-Hgb. o The hypocalcemia is directly related to the rate and volume of blood Tx. and a widened QRS. dextrose. and CVP o ECG changes: prolonged Q-T interval. o Treatment: CaCl  Acid–Base Changes  ? metabolic acidosis  2. acidosis. narrow pulse pressure. a prolonged PR interval. VEDP. coags  Microaggregate Delivery . hypovolemia. Impaired liver function or perfusion will lower the rate threshold for developing citrate intoxication.

creat. Sz Lab/DI CBC-D. heart block. CXR. neuropathy. F:M 2:1 A distorted anatomy with possible A/W obstruction  difficult A/W FOI B restrictive lung disease with pulmonary fibrosis C Arrhythmias. ABG. BUN.Sarcoidosis: Page 200 of 217  More common in African-American. CHF D on Steroid and immunosuppressant (stress dose) GI liver involvement CNS SOL. Lytes. PFT. LFT  Consider ICU backup if bad PFT . ECG.

B. CBC-D.  PTT and Liver enzymes and  CK  SARS serum Antibodies positive  SARS CoV isolation in cell culture  PCR positive for SARS CoV RNA Action:  Suspected Pt should be in resp isolation room ASAP if history contact with Pt with SARS or been in an epidemic area  During Pt transfer have a surgical mask over the Pt  Do CXR. pneumococcal .  PLT. and in a contact with resp secretion S/S and Lab:  Fever. other N&V. myalgia (nonspecific)  Nonproductive cough. diarrhea  Radiological evidence of pneumonia within 7-10 days of symptoms onset  Lab: lymphopenia. with SOB. headache. sputum for gram stain and C/S  Test for other respiratory pathogens inf A. pulse oxi. blood C/S. chills.SARS: Page 201 of 217  Not contagious until Pt become symptomatic with in 4-6 days(2-10)  Transmission by close contact. RSV.

C: calcinosis.Scleroderma Page 202 of 217  Progressive systemic sclerosis:Inflammation.  diffusion capacity C: risk of IHD.  LOS tone GERD need RSI B: A major cause of M&M. fibrosis of the conductive system arrhythmia. cardiomyopathy CHF. with systemic HTN  intravascular volume hypotension .  motility. Fibrosis of skin and viscera  Tissue edema  Some Pts have CREST syndrome. systemic and pulmonary HTN. S: scleroderma. Vascular sclerosis. Diffuse lung fibrosis restrictive lung disease. Age 20-40  Pregnancy  the progression of the disease in 50% of the Pt. R: Raynaud’s phenomenon. E: esophageal hypomotality. Chronic aspiration. A: flexion contracture difficult airway due to limited mouth opening. T: Telengectesia  F>M. pericarditis effusion  tamponade. Raynaud’s phenomenon in 70% risk of ischemia with art-line CNS: peripheral and cranial nerve neuropathy o Eye: conjunctivitis and corneal abrasion .

Echo if needed  OR: blood in the OR. PPC. ICU . ECG. Lytes. with that HR will . X-match. ABG. BUN. IV wormer  Position: prone check all pressure points.  risk of PPC (pneumonia. talk to the Pt regarding awake test  Lab:CBC-D. so consider -blockers  SSEP: if  latency by 10% or amp by 60%   BP. and frequent checking  May consider deliberate hypotension if there is no C/I. 1st anterior approach to release the anterior spinal artery. PFT. Heme). atelectasis) C myopathy. arrhythmias D avoid Sux Heme consider autologus blood donation pre-op  Consult (ICU. ask the surgeon to stop  Volatiles have the least effect on SSEP  See SSEP card  Post-op: pain. CXR. bear hugger.Scoliosis Sx Page 203 of 217  Need two stage Sx. creat. the 2nd stage to posterior  instrumentation  The scoliosis could be secondary to muscular disease ( muscular dystrophy) A Reflux RSI B Restrictive lung disease. Art-line. and diskectomy.

BAEP) are more resistance key points:  maintain a constant anesthetic level. PaO2 and PaCO2 Effect of inhalational agents:  SSEP  all  lat/amp. VEP) are more vulnerable to anesthetic drug effect  brain stem/subcortical (SSEP. except enf /. BP. with 0/ effect on the VEP and no effect on BAEP at regular doses Page 204 of 217 . and avoid any sudden changes or a bolus doses of any drugs  maintain and control other factors that may affect the SEP like temp.SEP  Any injury will cause  in latency &  amplitude  SSEP  50% in amp to surgical maneuver  significant  Cortical ( SSEP. N2O 0/  VEP  all lat/ amp  BAEP  alt/0 amp Effect of IV drugs:  All drugs  lat/ amp except ketamine and etomidate /.

SVR.Septic shock: Page 205 of 217 A LOC. lytes. Art-line. DIC Management:  ABC  ECG. D Abx. Sat. pul edema C low or high output failure. CVP/PAC. ARF Heme thrombocytopenia.. PT. ACTH stim test. D-dimer. frequent ABG. ARDS. if suspecting a source of infection do further investigation e. K. APC. base deficit. MAP >65.  Early goal directed therapy( CVP 8-12. creat. CBC-D. TEE or TTE for ? edocarditis.g. SvO2>70%)  Broad spectrum ABx . BUN. inotrops. Urine>0. adrenal insufficiency Renal ATN. full stomach B resp failure. ABG. and urine. steroids. vasopressors Met lactic acidosis. lytes disturbance. LFT.  Lab: CXR. ECG. Blood C/S. PTT.5ml/kg/hr. Fibrinogen. abdominal  CT…. sputum.

Class I Blood loss (ml) Blood loss (%) HR (per min) Blood pressure Pulse pressure RR Urine ml/hr Mental status 750 15 <100 Normal Normal or  14–20 30 Slightly anxious Class II 750–1500 15–30 >100 Normal  20–30 20–30 Mildly anxious Crystalloid Class III 1500–2000 30–40 >120   30–40 5–15 Anxious and confused Crystalloid + blood Page Class IV 206 of 217 2000 40 140   <35 Negligible Confused. lethargic Crystalloid + blood Fluid (3:1 rule)‡ Crystalloid .

and arthroscopy. and rotator cuff repair  Use of a beach chair position  VAE risk  Limited access to the airway tighten the connection. interscalene or combined  Assess the arm before doing the block for any neurological deficit  Risk of post-op neurological deficit  the level of the injury is at the level of the trunk (same as interscalene) difficult to determine the cause (surgical Vs block) Neurapraxia  90% resolve within 3-4 months . reinforce with tap  Possible eye and ears injury  Avoid excessive head rotation brachial plexus injury  Options GA.Shoulder Sx: Page 207 of 217  Arthroplasy.

The prognosis is related to the underlying cause of the syndrome. Pt with severe water intoxication associated with hyponatremia and mental confusion may require more aggressive therapy. with the iv administration of a hypertonic saline solution. pulmonary infections. Weight gain. Peripheral edema and hypertension are rare. This may be administered in conjunction with lasix Caution must be observed in patients with poor LV function. Isotonic saline is substituted for hypertonic solutions once the serum Na is in a safe range. . and mental confusion or convulsions are presenting symptoms. The diagnosis of the (SIADH) is one of exclusion.intracranial tumors. and a reduced urine output with a high osmolality.  serum osmolality. small cell carcinoma of the lung and hypothyroidism. Clinical manifestations occur as a result of a dilutional hyponatremia. and other causes of hyponatremia must first be ruled out. skeletal muscle weakness. Treatment: Pt with mild/mod H2O intoxication is restriction of fluid intake to 800 ml·day– 1 .    Inappropriate Secretion of Antidiuretic Hormone (SIADH) Page 208 of 217 Causes: head injuries.

 Ethnic background: Mediterranean and African-American. .  Pre-op you need to knew what is the result of the Hb electrophoresis. but at a greater risk of sickling.Sickle cell anemia Page 209 of 217  The defect in -chain.  In infancy Hb F is protective.   mortality with  in the number of the painful crisis in adult per-year. o Disease (severe) o Hb S > 75% may up to 95% o Could be associated with other abnormal Hb e.g severe hypoxemia.  % of Hb S o trait (mild) o < 50% is Hb S o sickling do not occur under normal physiological conditions o may happen under extreme conditions e. position 6  glutamic acid substituted by valine  3 types of crisis o hemolytic further anemia o sickling  pain & vaso-occlusive o Aplastic  may cause death.g Hb C o Pt with Hb SC have a normal Hb level.

and PCO2. ABx if suspect infection o Other consider Ventoline IV. pH. Isoprel/pei gtt. thiophylline. hypercarbia. keep the platue pressure < 30cmH2O o If need switch to pressure control o Also may consider Heliox o Be aware of AutoPEEP disconnect the bag. and paralyze o Ventilation: volume control Vt 6-10ml/kg. and respiratory/metabolic acidosis  Management: o ABC. ipratrupium bromide.Status asthmaticus Page 210 of 217  Emergency and life threatening  Result in respiratory failure with hypoxia. PEEP 5-10. if on vent  reverse ratio ventilation . 100% O2 o Intubate deep/ also may consider BiPAP o Ventoline. target normal PO2. Ketamine. leukotrine inhibitor. steroids. BNZ o Last volatile agent.

stimulator  resistance N   LOC. post-op  CEA. A. Echo D anti-PLT. Avoid Sux.fib.Stroke & TIA: Page 211 of 217  Hemorrhagic or ischemic  Etiology: Atherosclerosis. arrhythmias  ECG. A. loss of A/W reflux (RSI) B hypoventilation C HTN. and hyperglycemia  With chronic HTN the cerebral autoregulation curve shifted to the Rt . neuro deficit Peri-op  Avoid swinging in BP. severe HTN A  LOC. VHD. ASA.fib. coumadin. CAD. N. embolic  MI. VHD. trauma.

unilateral pupil dilation. creat. BUN. ECG  The main effect of Supratentorial masses is intracranial HTN  The main anesthetic goal is to maximize the therapeutic modality to  ICP. N&V. CVP. Avoid Sux  Maintenance: Isoflurane. and to avoid any factor that may  ICP  ICP control SEE ICP card  Monitoring: Standard + Art line. Foley cath. No N2O  Emergence: give Lidocaine IV 90 sec before extubation. assess for any neurological deficit . S/S of  ICP: headache. if CN involvement or  LOC.Supratentorial Intracranial Tumors Page 212 of 217  Review Pt overall medical condition  Focus on Neuro-evaluation:  LOC. lytes. with other standard induction drugs. for the art-line have the transducer at the level of external auditory meatus ( level of circle of Willis)  Induction: may need RSI. and consider using antihypertensive Meds(labetolol). and the presence and extent of focal neurological deficit  May have fluid and lytes abnormality  Review CT/MRI head  Lab: CBC. give Lidocaine IV. papilledema.

Hanti-phospholipid antibodies  thromboembolic complications. azathioprine. cardiac conduction abnormalities. stroke. clonidine. ECHO) D immunosuppressants (corticosteroids) or cytotoxic drugs (cyclophosphamide. isoniazid. enalapril. pneumonitis. and coronary arteritis. post-extubation edema B effusion. methyldopa. and peripheral neuropathy GI peritonitis. psychosis. stridor. pancreatitis. pul HTN. and alveolar hemorrhage.avoid Drug-induced lupus quinidine.  ventricular function. anemia R common cause of M&M in patients with SLE.(CXR. cyclosporine). Cardiomyopathy.Systemic Lupus Erythematosus Page 213 of 217 A cricoarytenoid arthritis  hoarseness. or airway obstruction (awake intubation). captopril. bowel ischemia. PFT) C pericardial effusion. noninfectious endocarditis (Libman-Sacks endocarditis)  mitral insufficiency (ECG. protein-losing enteropathy. tamponade. hydralazine. CRF CNS seizures. dementia. high correlation of pul HTN with Raynaud's phenomenon in patients with SLE. and lupoid hepatitis .

BP.  SV. SLE. lactic acidosis. fungal. CT . pulses paradoxus  Signs of systemic hypoprefusion: oliguria. cardiac herniation  ECG: diffuse ST-changes. HR. low voltage  Lab: ECG.  SBP. narrow pulse pressure.  CVP.Arthritis. CXR.Tamponade: Page 214 of 217  Emergency and life threatening  In acute as little as 200 ml cause S/S  In chronic up to 1000 ml cause S/S  Causes: o Infection: bacterial. RV infarction. TB o Inflammatory disease with vasculitis: R. myxedema o Radiation. viral. trauma. scleroderma o Metabolic: RF. Rt=Lt pressure  Dx by keeping in mind a high index of suspicion with clinical S/S and lab  Beck’s triad: hypotension. Echo. post-heart  Pathophysiology:  VEDV. malignancy.  CO. muffled heart sound  S/S: tachypnea. distended neck veins. Pul HTN. cool extr  DDx: tension Pneumo.

45-7. So no Atropine  Cardiac toxicity is the major cause of death  No correlation between serum level and symptom A  LOC  RSI B depression.  QT. seizure M metabolic acidosis  Management: o ABC o Gastric lavage o Activated charcoal 1g/kg with 60 ml sorbitol o Bicarb is the Key in the management 2 mEq/kg bolus then infusion 150mEq in 850 D5W to maintain pH 7.50 o For Vent arrhythmia give Lidocaine. and vasodilation by -blockade. hypotension due  contractility.1C are C/I o Hypotension  Norepi gtt o Bradycardia Isoprel or pacing No Atropine . ARDS C toxicity. arrest CNS hallucination.TCA overdose: Page 215 of 217  Gives anticholinergic syndrome. heart block. coma. sinus tach. Class 1A. wide QRS.

listen to the chest and initially intubate the Rt main bronchus. standard CAS monitors. Cap gas or VBG. have different size ETT.  Inhalation induction  bronch. metabolic acidosis  Worm up the room. not muscle relaxant until chest open. RDS. CXR.TEF Page 216 of 217  30% premature. the ligation of the fistula. associated CHD. pneumonia C CHD. if not stage repair.  Consider caudal epidural for post-op pain  Run maintenance fluids with glucose maintenance as well . then intubate after further mask ventilation to deepen the Pt. X-match with 2U peds in the room  Give atropine. ABG. and VATER. after intubation with the bevel directed posteriorly. and reanastomosis of the esophagus A subglottic stenosis B resp distress. Art-line  Lab CBC-D. with listening to the chest withdraw the tube slowly till you here bilateral breath sound. lytes. Echo. with insertion of G-tube under LA. VACTREL syndromes  Depend on the infant stability if stable complete repair. big IV. decompensation and CHF M dehydration.

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