Anesthesia For Children With Congenital Heart Disease1


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Anesthesia For Children With Congenital Heart Disease1

  1. 1. CHILDREN WITH CONGENITAL HEART DISEASE George Nicolaou, MD FRCPC Department of Anesthesia & Perioperative Medicine University of Western Ontario ANESTHESIA FOR
  2. 2. INTRODUCTION <ul><li>Number of children reaching adulthood with CHD has increased over the last 5 decades </li></ul><ul><li>D/T advances in diagnosis, medical, critical and surgical care </li></ul><ul><li>Therefore, not uncommon for adult patients with CHD to present for non-cardiac surgery </li></ul>
  3. 3. INCIDENCE <ul><li>7 to 10 per 1000 live births </li></ul><ul><li>Premature infants 2-3X higher incidence </li></ul><ul><li>Most common form of congenital disease </li></ul><ul><li>Accounts for 30% of total incidence of all congenital diseases </li></ul><ul><li>10% -15% have associated congenital anomalies of skeletal, RT, GUT or GIT </li></ul><ul><li>Only 15% survive to adulthood without treatment </li></ul>
  4. 4. ETIOLOGY <ul><li>10% associated with chromosomal abnormalities </li></ul><ul><li>Two thirds of these occur with Trisomy 21 </li></ul><ul><li>One third occur with karyotypic abnormalities such as Trisomy 13, Trisomy 18 & Turner Syndrome </li></ul><ul><li>Remaining 90% are multifactorial in origin </li></ul><ul><li>Interaction of several genes with or without external factors such as rubella, ethanol abuse, lithium and maternal diabetes mellitus </li></ul>
  5. 5. FETAL CIRCULATION <ul><li>There are 4 shunts in fetal circulation: placenta, ductus venosus, foramen ovale, and ductus arteriosus </li></ul><ul><li>In adult, gas exchange occurs in lungs. In fetus, the placenta provides the exchange of gases and nutrients </li></ul>
  6. 6. CARDIOPULMONARY CHANGES AT BIRTH <ul><li>Removal of placenta results in following: </li></ul><ul><li>↑ SVR (because the placenta has lowest vascular resistance in the fetus) </li></ul><ul><li>Cessation of blood flow in the umbilical vein resulting in closure of the ductus venosus </li></ul>
  7. 7. CARDIOPULMONARY CHANGES AT BIRTH <ul><li>Lung expansion -> reduction of the pulmonary vascular resistance (PVR), an increase in pulmonary blood flow, & a fall in PA pressure </li></ul>
  8. 8. CARDIOPULMONARY CHANGES AT BIRTH <ul><li>LUNG EXPANSION: </li></ul><ul><ul><li>Functional closure of the foramen ovale as a result ↑ LAP in excess RAP </li></ul></ul><ul><ul><li>The LAP increases as a result of the ↑ PBF and ↑ pulmonary venous return to the LA </li></ul></ul><ul><ul><li>RAP pressure falls as a result of closure of the ductus venosus </li></ul></ul><ul><ul><li>PDA closure D/T ↑ arterial oxygen saturation </li></ul></ul>
  9. 9. CARDIOPULMONARY CHANGES AT BIRTH <ul><li>PVR high as SVR near or at term </li></ul><ul><li>High PVR maintained by ↑ amount of smooth muscle in walls of pulmonary arterioles & alveolar hypoxia resulting from collapsed lungs </li></ul><ul><li>Lung expansion -> ↑ alveolar oxygen tension -> ↓ PVR </li></ul>
  10. 10. CLASSIFICATION OF CHD <ul><li>L – R SHUNTS </li></ul><ul><ul><li>Defects connecting arterial & venous circulation </li></ul></ul><ul><ul><li>SVR > PVR -> ↑ PBF </li></ul></ul><ul><ul><li>↑ p ulmonary blood flow -> pulmonary congestion -> CHF -> ↑ susceptibility to RTI </li></ul></ul><ul><ul><li>Long standing L-R shunts -> PHT </li></ul></ul><ul><ul><li>PVR > SVR -> R-L shunt -> Eisenmenger’s syndrome </li></ul></ul>
  11. 11. CLASSIFICATION OF CHD <ul><li>L - R SHUNTS INCLUDE : 5 </li></ul><ul><ul><li>ASD -> 7.5% of CHD </li></ul></ul><ul><ul><li>VSD -> COMMONEST CHD – 25% </li></ul></ul><ul><ul><li>PDA -> 7.5% of CHD </li></ul></ul><ul><ul><ul><li>Common in premature infants </li></ul></ul></ul><ul><ul><li>ENDOCARDIAL CUSHION DEFECT - 3% </li></ul></ul><ul><ul><ul><li>Often seen with trisomy 21( Common atrioventricular canal, Atrioventricular septal defect)[single Av annulus that drains boths atria] 3 components [Ostium primum+interventricular communication+abnormal AV valves} </li></ul></ul></ul><ul><ul><li>AORTOPULMONARY WINDOW [vascular communication between the ascending aorta and main pulm artery] </li></ul></ul>
  14. 14. L – R SHUNTS <ul><li>PERIOPERATIVE TREATMENT </li></ul><ul><ul><li>Indomethacin -> PDA closure </li></ul></ul><ul><ul><li>Digoxin, diuretics, ACE inhibitors -> CHF </li></ul></ul><ul><ul><li>Main PA band -> ↑ PVR -> ↓ L-R shunt </li></ul></ul><ul><ul><li>Definitive open heart surgery </li></ul></ul><ul><li>POSTOPERATIVE PROBLEMS </li></ul><ul><ul><li>SVTs and conduction delays </li></ul></ul><ul><ul><li>Valvular incompetence -> most common after canal defect repairs </li></ul></ul>
  15. 15. <ul><li>A subset of associated cardiac anomalies—so-called ductal-dependent lesions —depend on flow through the PDA to maintain systemic blood flow. Premature closure of the ductus without concurrent repair of the following defects is contraindicated and may be fatal: </li></ul><ul><li>Pulmonary artery hypoplasia </li></ul><ul><li>Pulmonary atresia </li></ul><ul><li>Tricuspid atresia </li></ul><ul><li>Transposition of the great arteries </li></ul><ul><li>Aortic valve atresia </li></ul><ul><li>Mitral valve atresia with hypoplastic left ventricle </li></ul><ul><li>Severe coarctation of the aorta/Interrupted aortic arch </li></ul>
  16. 16. CLASSIFICATION OF CHD <ul><li>R – L SHUNTS </li></ul><ul><ul><li>Resistance to pulmonary blood flow -> ↓ PBF -> hypoxemia and cyanosis </li></ul></ul><ul><ul><li>Defect between R and L heart </li></ul></ul><ul><li>INCLUDE : </li></ul><ul><ul><li>TOF – 10% of CHD, commonest R-L shunt </li></ul></ul><ul><ul><li>PULMONARY ATRESIA </li></ul></ul><ul><ul><li>TRICUSPID ATRESIA </li></ul></ul><ul><ul><li>EBSTEIN’S ANOMALY ( atrialized Rt Ventricle, proximal inlet portion of RV is above the displaced Tricuspid valve, also is stenosed usually.Associated with ASD, PS, or pulm atresia ,PDA and corrected TGA. Inc incidence of prexcitation syndrome[WPW] </li></ul></ul>
  17. 17. R – L SHUNTS <ul><li>GOAL -> ↑ PBF to improve oxygenation </li></ul><ul><ul><li>Neonatal PGE1 (0.03 – 0.10mcg/kg/min) maintains PDA -> ↑ PBF </li></ul></ul><ul><ul><li>PGE1 complications -> vasodilatation, hypotension, bradycardia, arrhythmias, apnea or hypoventilation, seizures, hyperthermia </li></ul></ul><ul><ul><li>Palliative shunts -> ↑ PBF, improve hypoxemia and stimulate growth in PA -> aids technical feasibility of future repair </li></ul></ul>
  18. 18. GLENN SHUNT
  20. 20. TETRALOGY OF FALLOT <ul><li>10% of all CHD </li></ul><ul><li>Most common R – L shunt </li></ul><ul><li>4 anomalies: </li></ul><ul><ul><li>RVOT obstruction ( infundibular, pulmonic or supravalvular stenosis ) </li></ul></ul><ul><ul><li>Subaortic VSD </li></ul></ul><ul><ul><li>Overriding aorta </li></ul></ul><ul><ul><li>RVH </li></ul></ul>
  22. 22. TETRALOGY OF FALLOT <ul><li>Hypercyanotic ( “tet” ) spells occur D/T infundibular spasm, low pH or low PaO2 </li></ul><ul><li>In awake patient manifests as acute cyanosis & hyperventilation </li></ul><ul><li>May occur with feeding, crying, defecation or stress </li></ul><ul><li>During anesthesia D/T acute dynamic infundibular spasm </li></ul>
  23. 23. TETRALOGY OF FALLOT <ul><li>Treatment of Hypercyanotic Spells </li></ul><ul><ul><li>High FiO2 -> pulmonary vasodilator -> ↓ PVR </li></ul></ul><ul><ul><li>Hydration (fluid bolus) -> opens RVOT </li></ul></ul><ul><ul><li>Morphine (0.1mg/kg/dose) -> sedation, ↓ PVR </li></ul></ul><ul><ul><li>Ketamine -> ↑ SVR, sedation, analgesia -> ↑ PBF </li></ul></ul><ul><ul><li>Phenylephrine (1mcg/kg/dose) -> ↑ SVR </li></ul></ul><ul><ul><li>β -blockers (Esmolol 100-200mcg/kg/min) </li></ul></ul><ul><li>-> ↓ HR,-ve inotropy -> improves flow across obstructed valve & ↓ infundibular spasm </li></ul>
  24. 24. TETRALOGY OF FALLOT <ul><li>Halothane -> ↓ HR & -ve inotropy </li></ul><ul><ul><li>Rapidly tuned on and off </li></ul></ul><ul><ul><li>Careful in severe RVF </li></ul></ul><ul><li>Thiopental -> -ve inotropy </li></ul><ul><li>Squatting, abdominal compression ->↑ SVR </li></ul>
  26. 26. CLASSIFICATION OF CHD <ul><li>COMPLEX SHUNTS (MIXING LESIONS) </li></ul><ul><ul><li>Continuous mixing of venous and arterial blood – blood saturation 70% - 80% </li></ul></ul><ul><ul><li>May or may not be obstruction to flow </li></ul></ul><ul><ul><li>Produce both cyanosis and CHF </li></ul></ul><ul><ul><li>Overzealous improvement in PBF steals circulation from aorta -> systemic hypotension -> coronary ischemia </li></ul></ul>
  27. 27. CLASSIFICATION OF CHD <ul><li>COMPLEX SHUNTS INCLUDE : </li></ul><ul><ul><li>T RUNCUS ARTERIOSUS(single arterial trunk arising from both ventricles,failure of the truncus to divide into aorta nd pulmonary artery)Always VSD </li></ul></ul><ul><ul><li>T RANSPOSITION OF GREAT VESSELS – 5% </li></ul></ul><ul><ul><ul><li>Arterial switch procedure > 95% survival (d-type) </li></ul></ul></ul><ul><ul><ul><li>L-type where both the 2 ventricles and the 2 great vessels are swaped(corrected TGA) </li></ul></ul></ul><ul><ul><li>T OTAL ANOMALOUS PV RETURN(all pulm viens drain into sys circ. Rather than lt atrium. Vertical vien then SVC, Supracardiac ,intracardiac in rt atrium ,or infracardiac in portal vien or IVC) </li></ul></ul><ul><ul><li>D OUBLE OUTLET RIGHT VENTRICLE(4 Types depending on the relation of the conotruncal VSD with the great vessels. </li></ul></ul><ul><ul><li>H YPOPLASTIC LEFT HEART SYNDROME </li></ul></ul><ul><ul><ul><li>Most common CHD presenting 1 st week of life </li></ul></ul></ul><ul><ul><ul><li>Most common cause of death in 1 st month of lif e </li></ul></ul></ul>
  28. 28. <ul><li>4 types of DORV 1.Subaortic VSD with or without pulmonary stenosis(like Fallots) </li></ul><ul><li>2Subpulmonary VSD with or without subaortic stenosis and or arch obstruction (like TGA </li></ul><ul><li>3Doubly comitted VSD </li></ul><ul><li>4.Remote VSD </li></ul>
  38. 38. CLASSIFICATION OF CHD <ul><li>OBSTRUCTIVE LESIONS </li></ul><ul><ul><li>Either valvular stenosis or vascular bands </li></ul></ul><ul><ul><li>↓ perfusion & pressure overload of corresponding ventricle </li></ul></ul><ul><ul><li>CHF common </li></ul></ul><ul><ul><li>Right sided obstructions   PBF  hypoxemia and cyanosis </li></ul></ul><ul><ul><li>Left sided obstructions   systemic blood flow  tissue hypoperfusion, metabolic acidosis and shock </li></ul></ul>
  39. 39. CLASSIFICATION OF CHD <ul><li>OBSTRUCTIVE LESIONS INCLUDE : </li></ul><ul><ul><li>AORTIC STENOSIS </li></ul></ul><ul><ul><li>MITRAL STENOSIS </li></ul></ul><ul><ul><li>PULMONIC STENOSIS </li></ul></ul><ul><ul><li>COARCTATION OF AORTA – 8% of CHD </li></ul></ul><ul><ul><ul><li>80% have bicuspid aortic valve </li></ul></ul></ul><ul><ul><li>COR TRIATRIATUM </li></ul></ul><ul><ul><li>INTERRUPTED AORTIC ARCH </li></ul></ul>
  46. 46. ANESTHETIC MANAGEMENT <ul><li>Perioperative management requires a team approach </li></ul><ul><li>Most important consideration is necessity for individualized care </li></ul><ul><li>CHD is polymorphic and may clinically manifest across a broad clinical spectrum </li></ul>
  47. 47. ANESTHETIC MANAGEMENT <ul><li>Unpalliated </li></ul><ul><li>Partially palliated </li></ul><ul><li>Completely palliated </li></ul><ul><ul><li>ASD and PDA only congenital lesions that can be truly “corrected” </li></ul></ul>Anesthesiologists will encounter children with CHD for elective non-cardiac surgery at one of three stages:
  48. 48. ANESTHETIC MANAGEMENT <ul><li>50% Dx by 1 st week of life; rest by 5 years </li></ul><ul><li>Child’s diagnosis & current medical condition will determine preoperative evaluation </li></ul><ul><li>Understand the anatomic and hemodynamic function of child’s heart </li></ul><ul><li>Discuss case with pediatrician and cardiologist </li></ul><ul><li>Review diagnostic & therapeutic interventions </li></ul><ul><li>Above will estimate disease severity and help formulate anesthetic plan </li></ul>
  49. 49. HISTORY & PHYSICAL <ul><li>Assess functional status – daily activities & exercise tolerance </li></ul><ul><li>Infants - ↓ cardiac reserve -> cyanosis, diaphoresis & respiratory distress during feeding </li></ul><ul><li>Palpitations, syncope, chest pain </li></ul><ul><li>Heart murmur (s) </li></ul><ul><li>Congestive heart failure </li></ul><ul><li>Hypertension </li></ul>
  50. 50. HISTORY & PHYSICAL <ul><li>Tachypnea, dyspnea, cyanosis </li></ul><ul><li>Squatting </li></ul><ul><li>Clubbing of digits </li></ul><ul><li>FTT d/t limited cardiac output and increased oxygen consumption </li></ul><ul><li>Medications – diuretics, afterload reduction agents, antiplatelet, anticoagulants </li></ul><ul><li>Immunosuppressants – heart transplant </li></ul>
  51. 51. LABORATORY EVALUATION <ul><ul><li>BLOODWORK </li></ul></ul><ul><ul><ul><li>Electrolyte disturbances 2° to chronic diuretic therapy or renal dysfunction </li></ul></ul></ul><ul><ul><ul><li>Hemoglobin level best indicator of R-L shunting magnitude & chronicity </li></ul></ul></ul><ul><ul><ul><li>Hematocrit to evaluate severity of polycythemia or iron deficiency anemia </li></ul></ul></ul><ul><ul><ul><li>Screening coagulation tests </li></ul></ul></ul><ul><ul><ul><li>Baseline ABG & pulse oximetry </li></ul></ul></ul><ul><ul><ul><li>Calcium & glucose - newborns, critically ill children </li></ul></ul></ul>
  52. 52. LABORATORY EVALUATION <ul><li>12 LEAD EKG </li></ul><ul><ul><li>Chamber enlargement/hypertrophy </li></ul></ul><ul><ul><li>Axis deviation </li></ul></ul><ul><ul><li>Conduction defects </li></ul></ul><ul><ul><li>Arrhythmias </li></ul></ul><ul><ul><li>Myocardial ischemia </li></ul></ul>
  53. 53. LABORATORY EVALUATION <ul><li>CHEST X - RAY </li></ul><ul><ul><li>Heart size and shape </li></ul></ul><ul><ul><li>Prominence of pulmonary vascularity </li></ul></ul><ul><ul><li>Lateral film if previous cardiac surgery for position of major vessels in relation to sternum </li></ul></ul>
  54. 54. LABORATORY EVALUATION <ul><li>ECHOCARDIOGRAPHY </li></ul><ul><ul><li>Anatomic defects/shunts </li></ul></ul><ul><ul><li>Ventricular function </li></ul></ul><ul><ul><li>Valve function </li></ul></ul><ul><ul><li>Doppler & color flow imaging  direction of flow through defect/valves, velocities and pressure gradients </li></ul></ul>
  55. 55. LABORATORY EVALUATION <ul><li>CARDIAC CATHERIZATION </li></ul><ul><ul><li>Size & location of defects </li></ul></ul><ul><ul><li>Degree of stenosis & shunt </li></ul></ul><ul><ul><li>Pressure gradients & O 2 saturation in each chamber and great vessel </li></ul></ul><ul><ul><li>Mixed venous O 2 saturation obtained in SVC or proximal to area where shunt occurs </li></ul></ul><ul><ul><li>Low saturations in LA and LV = R – L shunt </li></ul></ul><ul><ul><li>High saturations in RA & RV = L – R shunt </li></ul></ul>
  56. 56. LABORATORY EVALUATION <ul><li>CARDIAC CATHERIZATION </li></ul><ul><ul><li>Determine shunt direction: ratio of pulmonary to systemic blood flow : Qp / Qs </li></ul></ul><ul><ul><li>Qp / Qs ratio < 1= R – L shunt </li></ul></ul><ul><ul><li>Qp / Qs ratio > 1= L – R shunt </li></ul></ul>
  57. 57. PREMEDICATION <ul><li>Omit for infants < six months of age </li></ul><ul><li>Administer under direct supervision of Anesthesiologist in preoperative facility </li></ul><ul><li>Oxygen, ventilation bag, mask and pulse oximetry immediately available </li></ul><ul><li>Oral Premedication </li></ul><ul><ul><ul><li>Midazolam 0.25 -1.0 mg/kg </li></ul></ul></ul><ul><ul><ul><li>Ketamine 2 - 4 mg/kg </li></ul></ul></ul><ul><ul><ul><li>Atropine 0.02 mg/kg </li></ul></ul></ul>
  58. 58. PREMEDICATION <ul><li>IV Premedication </li></ul><ul><ul><ul><li>Midazolam 0.02 - 0.05 mg/kg titrated in small increments </li></ul></ul></ul><ul><li>IM Premedication </li></ul><ul><ul><ul><li>Uncooperative or unable to take orally </li></ul></ul></ul><ul><ul><ul><li>Ketamine 1-2 mg/kg </li></ul></ul></ul><ul><ul><ul><li>Midazolam 0.2 mg/kg </li></ul></ul></ul><ul><ul><ul><li>Glycopyrrolate or Atropine 0.02 mg/kg </li></ul></ul></ul>
  59. 59. MONITORING <ul><li>Routine CAS monitoring </li></ul><ul><li>Precordial or esophageal stethoscope </li></ul><ul><li>Continuous airway manometry </li></ul><ul><li>Multiple - site temperature measurement </li></ul><ul><li>Volumetric urine collection </li></ul><ul><li>Pulse oximetry on two different limbs </li></ul><ul><li>TEE </li></ul>
  60. 60. MONITORING <ul><li>PDA </li></ul><ul><ul><li>Pulse oximetry right hand to measure pre-ductal oxygenation </li></ul></ul><ul><ul><li>2 nd probe on toe to measure post-ductal oxygenation </li></ul></ul><ul><li>COARCTATION OF AORTA </li></ul><ul><ul><li>Pulse oximeter on right upper limb </li></ul></ul><ul><ul><li>Pre and post - coarctation blood pressure cuffs should be placed </li></ul></ul>
  61. 61. ANESTHETIC AGENTS <ul><li>INHALATIONAL AGENTS </li></ul><ul><ul><li>Safe in children with minor cardiac defects </li></ul></ul><ul><ul><li>Most common agents used are halothane and sevoflurane in oxygen </li></ul></ul><ul><ul><li>Monitor EKG for changes in P wave  retrograde P wave or junctional rhythm may indicate too deep anesthesia </li></ul></ul>
  62. 62. INHALATIONAL ANESTHETICS <ul><li>HALOTHANE </li></ul><ul><ul><li>Depresses myocardial function, alters sinus node function, sensitizes myocardium to catecholamines </li></ul></ul><ul><ul><li> MAP +  HR </li></ul></ul><ul><ul><li> CI +  EF </li></ul></ul><ul><li>Relax infundibular spasm in TOF </li></ul><ul><li>Agent of choice for HCOM </li></ul>
  63. 63. INHALATIONAL ANESTHETICS <ul><li>SEVOFLURANE </li></ul><ul><li>No  HR </li></ul><ul><li>Less myocardial depression than Halothane </li></ul><ul><li>Mild  SVR -> improves systemic flow in L-R shunts </li></ul><ul><li>Can produce diastolic dysfunction </li></ul>
  64. 64. INHALATIONAL ANESTHETICS <ul><li>ISOFLURANE </li></ul><ul><li>Pungent  not good for induction </li></ul><ul><li>Incidence of laryngospasm > 20% </li></ul><ul><li>Less myocardial depression than Halothane </li></ul><ul><li>Vasodilatation leads to  SVR ->  MAP </li></ul><ul><li> HR which can lead to  CI </li></ul>
  65. 65. INHALATIONAL ANESTHETICS <ul><li>DESFLURANE </li></ul><ul><li>Pungent  not good for induction; highest incidence of laryngospasm </li></ul><ul><li>SNS activation ->  with fentanyl </li></ul><ul><li> HR +  SVR </li></ul><ul><li>Less myocardial depression than Halothane </li></ul>
  66. 66. INHALATIONAL ANESTHETICS <ul><li>NITROUS OXIDE </li></ul><ul><li>Enlarge intravascular air emboli </li></ul><ul><li>May cause microbubbles and macrobubbles to expand   obstruction to blood flow in arteries and capillaries </li></ul><ul><li>In shunts, potential for bubbles to be shunted into systemic circulation </li></ul>
  67. 67. INHALATIONAL ANESTHETICS <ul><li>NITROUS OXIDE </li></ul><ul><li>At 50% concentration does not affect PVR and PAP in children </li></ul><ul><li>Mildly  CO at 50% concentration </li></ul><ul><li>Avoid in children with limited pulmonary blood flow, PHT or  myocardial function </li></ul>
  68. 68. IM & IV ANESTHETICS <ul><li>KETAMINE </li></ul><ul><li>No change in PVR in children when airway maintained & ventilation supported </li></ul><ul><li>Sympathomimetic effects help maintain HR, SVR, MAP and contractility </li></ul><ul><li>Greater hemodynamic stability in hypovolemic patients </li></ul><ul><li>Copious secretions -> laryngospasm -> atropine or glycopyrrolate </li></ul>
  69. 69. IM & IV ANESTHETICS <ul><li>KETAMINE </li></ul><ul><li>Relative contraindications may be coronary insufficiency caused by: </li></ul><ul><ul><li>anomalous coronary artery </li></ul></ul><ul><ul><li>severe critical AS </li></ul></ul><ul><ul><li>hypoplastic left heart syndrome with aortic atresia </li></ul></ul><ul><ul><li>hypoplasia of the ascending aorta </li></ul></ul><ul><li>Above patients prone to VF d/t coronary insufficiency d/t catecholamine release from ketamine </li></ul>
  70. 70. IM & IV ANESTHETICS <ul><li>IM Induction with Ketamine: </li></ul><ul><li>Ketamine 5 mg/kg </li></ul><ul><li>Succinylcholine 5 mg/kg or Rocuronium 1.5 – 2.0 mg/kg </li></ul><ul><li>Atropine or Glycopyrrolate 0.02 mg/kg </li></ul><ul><li>IV Induction with Ketamine: </li></ul><ul><li>Ketamine 1-2 mg/kg </li></ul><ul><li>Succinylcholine 1-2 mg/kg or Rocuronium 0.6-1.2 mg/kg </li></ul><ul><li>Atropine or Glycopyrrolate 0.01 mg/kg </li></ul>
  71. 71. IM & IV ANESTHETICS <ul><li>OPIOIDS </li></ul><ul><li>Excellent induction agents in very sick children </li></ul><ul><li>No cardiodepressant effects if bradycardia avoided </li></ul><ul><li>If used with N 2 O - negative inotropic effects of N 2 O may appear </li></ul><ul><li>Fentanyl 25-100 µg/kg IV </li></ul><ul><li>Sufentanil 5-20 µg/kg IV </li></ul><ul><li>Pancuronium 0.05 - 0.1 mg/kg IV  offset vagotonic effects of high dose opioids </li></ul>
  72. 72. IM & IV ANESTHETICS <ul><li>ETOMIDATE </li></ul><ul><li>CV stability </li></ul><ul><li>0.3 mg/kg IV </li></ul><ul><li>THIOPENTAL & PROPOFOL </li></ul><ul><li>Not recommended in patients with severe cardiac defects </li></ul><ul><li>In moderate cardiac defects: </li></ul><ul><ul><li>Thiopental 1-2 mg/kg IV or Propofol 1-1.5 mg/kg IV </li></ul></ul><ul><ul><li>Patient euvolemic </li></ul></ul>
  73. 73. ANESTHETIC MANAGEMENT <ul><li>GENERAL PRINCIPLES </li></ul><ul><li>Where: </li></ul><ul><li>Q = Blood flow (CO) </li></ul><ul><li>P = Pressure within a chamber or vessel </li></ul><ul><li>R = Vascular resistance of pulmonary or systemic vasculature </li></ul><ul><li>Ability to alter above relationship is the basic tenet of anesthetic management in children with CHD </li></ul>
  74. 74. ANESTHETIC MANAGEMENT <ul><li>P  manipulate with positive or negative inotropic agents </li></ul><ul><li>Q  hydration +  preload and inotropes </li></ul><ul><li>However, the anesthesiologist’s principal focus is an attempt to manipulate resistance, by dilators and constrictors </li></ul>
  75. 75. ANESTHETIC MANAGEMENT <ul><li>GENERAL CONSIDERATIONS </li></ul><ul><ul><li>De-air intravenous lines air bubble in a R-L shunt can cross into systemic circulation and cause a stroke </li></ul></ul><ul><ul><li>L-R shunt air bubbles pass into lungs and are absorbed </li></ul></ul><ul><ul><li>Endocarditis prophylaxis </li></ul></ul><ul><ul><li>Tracheal narrowing d/t subglottic stenosis or associated vascular malformations </li></ul></ul>
  76. 76. ANESTHETIC MANAGEMENT <ul><ul><li>Tracheal shortening or stenosis esp. in children with trisomy 21 </li></ul></ul><ul><ul><li>Strokes from embolic phenomena in R-L shunts and polycythemia </li></ul></ul><ul><ul><li>Chronic hypoxemia compensated by polycythemia -> ↑ O2 carrying capacity </li></ul></ul><ul><ul><li>HCT ≥ 65% -> ↑ blood viscosity -> tissue hypoxia & ↑ SVR & PVR -> venous thrombosis -> strokes & cardiac ischemia </li></ul></ul>
  77. 77. ANESTHETIC MANAGEMENT <ul><ul><li>Normal or low HCT D/T iron deficiency -> less deformable RBCs -> ↑ blood viscosity </li></ul></ul><ul><ul><li>Therefore adequate hydration & decrease RBC mass if HCT > 65% </li></ul></ul><ul><ul><li>Diuretics -> hypochloremic, hypokalemic metabolic alkalosis </li></ul></ul>
  78. 78. ANESTHETIC MANAGEMENT <ul><li>ANESTHESIA INDUCTION </li></ul><ul><li>Myocardial function preserved  IV or inhalational techniques suitable </li></ul><ul><li>Severe cardiac defects  IV induction </li></ul><ul><li>Modify dosages in patients with severe failure </li></ul>
  79. 79. ANESTHESIC MANAGEMENT <ul><li>ANESTHESIA MAINTENANCE </li></ul><ul><li>Depends on preoperative status </li></ul><ul><li>Response to induction & tolerance of individual patient </li></ul><ul><li>Midazolam 0.15-0.2 mg/IV for amnesia </li></ul>
  80. 80. ANESTHETIC MANAGEMENT <ul><li>L - R SHUNTS : </li></ul><ul><ul><li>Continuous dilution in pulmonary circulation may  onset time of IV agents </li></ul></ul><ul><ul><li>Speed of induction with inhalation agents not affected unless CO is significantly reduced </li></ul></ul><ul><ul><li>Degree of RV overload and/or failure underappreciated – careful induction </li></ul></ul>
  81. 81. ANESTHETIC MANAGEMENT <ul><li>L-R SHUNTS : </li></ul><ul><ul><li>GOAL =  SVR and ↑ PVR ->  L-R shunt </li></ul></ul><ul><ul><ul><li>PPV & PEEP increases PVR </li></ul></ul></ul><ul><ul><ul><li>Ketamine increases SVR </li></ul></ul></ul><ul><ul><ul><li>Inhalation agents decrease SVR </li></ul></ul></ul>
  82. 82. ANESTHETIC MANAGEMENT <ul><li>R-L SHUNTS : </li></ul><ul><ul><li>GOAL :  PBF by  SVR and ↓ PVR </li></ul></ul><ul><ul><li> PVR & ↓ SVR -> ↓ PBF </li></ul></ul><ul><ul><ul><ul><li>Hypoxemia/atelectasis/PEEP </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Acidosis/hypercapnia </li></ul></ul></ul></ul><ul><ul><ul><ul><li> HCT </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Sympathetic stimulation & surgical stimulation </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Vasodilators & inhalation agents -> ↓ SVR </li></ul></ul></ul></ul>
  83. 83. ANESTHETIC MANAGEMENT <ul><li>↓ PVR &  SVR ->  PBF </li></ul><ul><ul><li>Hyperoxia/Normal FRC </li></ul></ul><ul><ul><li>Alkalosis/hypocapnia </li></ul></ul><ul><ul><li>Low HCT </li></ul></ul><ul><ul><li>Low mean airway pressure </li></ul></ul><ul><ul><li>Blunted stress response </li></ul></ul><ul><ul><li>Nitric oxide/ pulmonary vasodilators </li></ul></ul><ul><ul><li>Vasoconstrictors & direct manipulation ->  SVR </li></ul></ul>
  84. 84. ANESTHETIC MANAGEMENT <ul><li>R –L SHUNTS : </li></ul><ul><ul><li>Continue PE 1 infusions </li></ul></ul><ul><ul><li>Adequate hydration esp. if HCT > 50% </li></ul></ul><ul><ul><li>Inhalation induction prolonged by limited pulmonary blood flow </li></ul></ul><ul><ul><li>IV induction times are more rapid d/t bypassing pulmonary circulation dilution </li></ul></ul><ul><ul><li>PEEP and PPV increase PVR </li></ul></ul>
  85. 85. ANESTHETIC MANAGEMENT <ul><li>COMPLEX SHUNTS : </li></ul><ul><ul><li>Manipulating PVR or SVR to  PBF will: </li></ul></ul><ul><ul><ul><li>Not improve oxygenation </li></ul></ul></ul><ul><ul><ul><li>Worsen biventricular failure </li></ul></ul></ul><ul><ul><ul><li>Steal circulation from aorta and cause coronary ischemia </li></ul></ul></ul><ul><ul><li>Maintain “status” quo with high dose opioids that do not significantly affect heart rate, contractibility, or resistance is recommended </li></ul></ul>
  86. 86. ANESTHETIC MANAGEMENT <ul><li>COMPLEX SHUNTS : </li></ul><ul><ul><li>Short procedures slow gradual induction with low dose Halothane least effect on +ve chronotropy & SVR </li></ul></ul><ul><ul><li>Nitrous Oxide limits FiO2 & helps prevent coronary steal & ↓ Halothane requirements </li></ul></ul>
  87. 87. ANESTHETIC MANAGEMENT <ul><li>OBSTRUCTIVE LESIONS </li></ul><ul><ul><li>Lesions with > 50 mmHg pressure gradient + CHF  opioid technique </li></ul></ul><ul><ul><li>Optimize preload  improves flow beyond lesion </li></ul></ul><ul><ul><li>Avoid tachycardia  ↑ myocardial demand & ↓ flow beyond obstruction </li></ul></ul><ul><ul><li>Inhalation agents  -ve inotropy & decrease SVR  worsens gradient & flow past obstruction </li></ul></ul>
  88. 88. REGIONAL ANESTHESIA &ANALGESIA <ul><li>CONSIDERATIONS </li></ul><ul><ul><li>Coarctation of aorta  dilated tortuous intercostal collateral arteries   risk for arterial puncture and  absorption of local anesthetic during intercostal blockade </li></ul></ul><ul><ul><li>Lungs may absorb up to 80% of local anesthetic on first passage. Therefore  risk of local anesthetic toxicity in R-L shunts </li></ul></ul>
  89. 89. <ul><li>Central axis blockade may cause vasodilation which can: </li></ul><ul><ul><ul><li>Be hazardous in patients with significant AS or left-sided obstructive lesions </li></ul></ul></ul><ul><ul><ul><li>Cause  oxyhemoglobin saturation in R-L shunts </li></ul></ul></ul><ul><ul><ul><li>Improve microcirculation flow and  venous thrombosis in patients with polycythemia </li></ul></ul></ul>REGIONAL ANESTHESIA &ANALGESIA <ul><li>Children with chronic cyanosis are at risk for coagulation abnormalities </li></ul>
  90. 90. POSTOPERATIVE MANAGEMENT <ul><li>Children with CHD are very susceptible to: </li></ul><ul><ul><ul><li>Deleterious effects of hypoventilation </li></ul></ul></ul><ul><ul><ul><li>Mild decreases in oxyhemoglobin saturation </li></ul></ul></ul><ul><li>Therefore, give supplemental O 2 and maintain patent airway </li></ul><ul><li>In patients with single ventricle titrate SaO 2 to 85%. Higher oxygen saturations can  PVR  PBF   systemic blood flow </li></ul>
  91. 91. <ul><li>Pain   catecholamines which can affect vascular resistance and shunt direction </li></ul><ul><li>Anticipate conduction disturbances in septal defects </li></ul><ul><li>Pain  infundibular spasm in TOF  RVOT obstruction  cyanosis, hypoxia, syncope, seizures, acidosis and death </li></ul>POSTOPERATIVE MANAGEMENT