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Anesthesia for children with Congenital Heart Disease

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Presented at Egyptian Pediatric Anesthesia Conference held at Cairo, Egypt. www.egyptpac.org

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Anesthesia for children with Congenital Heart Disease

  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 • Number of children reaching adulthood with CHD has increased over the last 5 decades • D/T advances in diagnosis, medical, critical and surgical care • Therefore, not uncommon for adult patients with CHD to present for non-cardiac surgery
  3. 3. INCIDENCE • 7 to 10 per 1000 live births • Premature infants 2-3X higher incidence • Most common form of congenital disease • Accounts for 30% of total incidence of all congenital diseases • 10% -15% have associated congenital anomalies of skeletal, RT, GUT or GIT • Only 15% survive to adulthood without treatment
  4. 4. ETIOLOGY • 10% associated with chromosomal abnormalities • Two thirds of these occur with Trisomy 21 • One third occur with karyotypic abnormalities such as Trisomy 13, Trisomy 18 & Turner Syndrome • Remaining 90% are multifactorial in origin • Interaction of several genes with or without external factors such as rubella, ethanol abuse, lithium and maternal diabetes mellitus
  5. 5. FETAL CIRCULATION • There are 4 shunts in fetal circulation: placenta, ductus venosus, foramen ovale, and ductus arteriosus • In adult, gas exchange occurs in lungs. In fetus, the placenta provides the exchange of gases and nutrients
  6. 6. CARDIOPULMONARY CHANGES AT BIRTH • Removal of placenta results in following: • ↑ SVR (because the placenta has lowest vascular resistance in the fetus) • Cessation of blood flow in the umbilical vein resulting in closure of the ductus venosus
  7. 7. CARDIOPULMONARY CHANGES AT BIRTH • Lung expansion → reduction of the pulmonary vascular resistance (PVR), an increase in pulmonary blood flow, & a fall in PA pressure
  8. 8. CARDIOPULMONARY CHANGES AT BIRTH • LUNG EXPANSION: – Functional closure of the foramen ovale as a result ↑ LAP in excess RAP – The LAP increases as a result of the ↑ PBF and ↑ pulmonary venous return to the LA – RAP pressure falls as a result of closure of the ductus venosus – PDA closure D/T ↑ arterial oxygen saturation
  9. 9. CARDIOPULMONARY CHANGES AT BIRTH • PVR high as SVR near or at term • High PVR maintained by ↑ amount of smooth muscle in walls of pulmonary arterioles & alveolar hypoxia resulting from collapsed lungs • Lung expansion → ↑ alveolar oxygen tension → ↓ PVR
  10. 10. CLASSIFICATION OF CHD • L – R SHUNTS – Defects connecting arterial & venous circulation – SVR > PVR → ↑ PBF – ↑ pulmonary blood flow → pulmonary congestion → CHF → ↑ susceptibility to RTI – Long standing L-R shunts → PHT – PVR > SVR → R-L shunt → Eisenmenger’s syndrome
  11. 11. CLASSIFICATION OF CHD • L - R SHUNTS INCLUDE : – ASD →7.5% of CHD – VSD → COMMONEST CHD – 25% – PDA → 7.5% of CHD • Common in premature infants – ENDOCARDIAL CUSHION DEFECT - 3% • Often seen with trisomy 21 – AORTOPULMONARY WINDOW
  12. 12. VENTRICULAR SEPTAL DEFECT
  13. 13. ATRIOVENTRICULAR CANAL DEFECT
  14. 14. L – R SHUNTS • PERIOPERATIVE TREATMENT – Indomethacin → PDA closure – Digoxin, diuretics, ACE inhibitors → CHF – Main PA band → ↑ PVR → ↓ L-R shunt – Definitive open heart surgery • POSTOPERATIVE PROBLEMS – SVTs and conduction delays – Valvular incompetence → most common after canal defect repairs
  15. 15. CLASSIFICATION OF CHD • R – L SHUNTS – Defect between R and L heart – Resistance to pulmonary blood flow → ↓ PBF → hypoxemia and cyanosis • INCLUDE : – TOF – 10% of CHD, commonest R-L shunt – PULMONARY ATRESIA – TRICUSPID ATRESIA – EBSTEIN’S ANOMALY
  16. 16. R – L SHUNTS • GOAL → ↑ PBF to improve oxygenation – Neonatal PGE1 (0.03 – 0.10mcg/kg/min) maintains PDA → ↑ PBF – PGE1 complications → vasodilatation, hypotension, bradycardia, arrhythmias, apnea or hypoventilation, seizures, hyperthermia – Palliative shunts → ↑ PBF, improve hypoxemia and stimulate growth in PA → aids technical feasibility of future repair
  17. 17. GLENN SHUNT
  18. 18. MODIFIED BLALOCK-TAUSSIG SHUNT
  19. 19. TETRALOGY OF FALLOT • 10% of all CHD • Most common R – L shunt • 4 anomalies: – RVOT obstruction ( infundibular, pulmonic or supravalvular stenosis ) – Subaortic VSD – Overriding aorta – RVH
  20. 20. TETRALOGY OF FALLOT
  21. 21. TETRALOGY OF FALLOT • Hypercyanotic ( “tet” ) spells occur D/T infundibular spasm, low pH or low PaO2 • In awake patient manifests as acute cyanosis & hyperventilation • May occur with feeding, crying, defecation or stress • During anesthesia D/T acute dynamic infundibular spasm
  22. 22. TETRALOGY OF FALLOT • Treatment of Hypercyanotic Spells – High FiO2 → pulmonary vasodilator → ↓ PVR – Hydration (fluid bolus) → opens RVOT – Morphine (0.1mg/kg/dose) → sedation,↓ PVR – Ketamine → ↑ SVR, sedation, analgesia → ↑ PBF – Phenylephrine (1mcg/kg/dose) → ↑ SVR – β-blockers (Esmolol 100-200mcg/kg/min) → ↓HR,-ve inotropy → improves flow across obstructed valve &↓ infundibular spasm
  23. 23. TETRALOGY OF FALLOT • Halothane → ↓ HR & -ve inotropy – Rapidly tuned on and off – Careful in severe RVF • Thiopental → -ve inotropy • Squatting, abdominal compression→↑ SVR
  24. 24. EBSTEIN’S ANOMALY
  25. 25. CLASSIFICATION OF CHD • COMPLEX SHUNTS (MIXING LESIONS) – Continuous mixing of venous and arterial blood – blood saturation 70% - 80% – May or may not be obstruction to flow – Produce both cyanosis and CHF – Overzealous improvement in PBF steals circulation from aorta → systemic hypotension → coronary ischemia
  26. 26. CLASSIFICATION OF CHD • COMPLEX SHUNTS INCLUDE : – TRUNCUS ARTERIOSUS – TRANSPOSITION OF GREAT VESSELS – 5% • Arterial switch procedure > 95% survival – TOTAL ANOMALOUS PV RETURN – DOUBLE OUTLET RIGHT VENTRICLE – HYPOPLASTIC LEFT HEART SYNDROME • Most common CHD presenting 1st week of life • Most common cause of death in 1st month of life
  27. 27. TOTAL ANOMALOUS PULMONARY VENOUS RETURN
  28. 28. TOTAL ANOMALOUS PULMONARY VENOUS RETURN
  29. 29. HYPOPLASTIC LEFT HEART SYNDROME
  30. 30. TRANSPOSITION OF GREAT VESSELS
  31. 31. TRUNCUS ARTERIOSUS
  32. 32. DOUBLE OUTLET RIGHT VENTRICLE
  33. 33. FONTAN PROCEDURE
  34. 34. NORWOOD PROCEDURE
  35. 35. JATENE PROCEDURE
  36. 36. CLASSIFICATION OF CHD • OBSTRUCTIVE LESIONS – Either valvular stenosis or vascular bands – ↓ perfusion & pressure overload of corresponding ventricle – CHF common – Right sided obstructions   PBF  hypoxemia and cyanosis – Left sided obstructions   systemic blood flow  tissue hypoperfusion, metabolic acidosis and shock
  37. 37. CLASSIFICATION OF CHD • OBSTRUCTIVE LESIONS INCLUDE : – AORTIC STENOSIS – MITRAL STENOSIS – PULMONIC STENOSIS – COARCTATION OF AORTA – 8% of CHD • 80% have bicuspid aortic valve – COR TRIATRIATUM – INTERRUPTED AORTIC ARCH
  38. 38. COARCTATION OF AORTA
  39. 39. COARCTATION OF AORTA
  40. 40. INTERUPTION OF AORTIC ARCH
  41. 41. COR TRIATIATUM
  42. 42. CLASSIFICATION OF CHD
  43. 43. CLASSIFICATION OF CHD
  44. 44. ANESTHETIC MANAGEMENT • Perioperative management requires a team approach • Most important consideration is necessity for individualized care • CHD is polymorphic and may clinically manifest across a broad clinical spectrum
  45. 45. ANESTHETIC MANAGEMENT • Unpalliated • Partially palliated • Completely palliated – ASD and PDA only congenital lesions that can be truly “corrected” Anesthesiologists will encounter children with CHD for elective non-cardiac surgery at one of three stages:
  46. 46. ANESTHETIC MANAGEMENT • 50% Dx by 1st week of life; rest by 5 years • Child’s diagnosis & current medical condition will determine preoperative evaluation • Understand the anatomic and hemodynamic function of child’s heart • Discuss case with pediatrician and cardiologist • Review diagnostic & therapeutic interventions • Above will estimate disease severity and help formulate anesthetic plan
  47. 47. HISTORY & PHYSICAL • Assess functional status – daily activities & exercise tolerance • Infants - ↓ cardiac reserve → cyanosis, diaphoresis & respiratory distress during feeding • Palpitations, syncope, chest pain • Heart murmur (s) • Congestive heart failure • Hypertension
  48. 48. HISTORY & PHYSICAL • Tachypnea, dyspnea, cyanosis • Squatting • Clubbing of digits • FTT d/t limited cardiac output and increased oxygen consumption • Medications – diuretics, afterload reduction agents, antiplatelet, anticoagulants • Immunosuppressants – heart transplant
  49. 49. LABORATORY EVALUATION • BLOODWORK • Electrolyte disturbances 2° to chronic diuretic therapy or renal dysfunction • Hemoglobin level best indicator of R-L shunting magnitude & chronicity • Hematocrit to evaluate severity of polycythemia or iron deficiency anemia • Screening coagulation tests • Baseline ABG & pulse oximetry • Calcium & glucose - newborns, critically ill children
  50. 50. LABORATORY EVALUATION • 12 LEAD EKG – Chamber enlargement/hypertrophy – Axis deviation – Conduction defects – Arrhythmias – Myocardial ischemia
  51. 51. LABORATORY EVALUATION • CHEST X - RAY – Heart size and shape – Prominence of pulmonary vascularity – Lateral film if previous cardiac surgery for position of major vessels in relation to sternum
  52. 52. LABORATORY EVALUATION • ECHOCARDIOGRAPHY – Anatomic defects/shunts – Ventricular function – Valve function – Doppler & color flow imaging  direction of flow through defect/valves, velocities and pressure gradients
  53. 53. LABORATORY EVALUATION • CARDIAC CATHERIZATION – Size & location of defects – Degree of stenosis & shunt – Pressure gradients & O2 saturation in each chamber and great vessel – Mixed venous O2 saturation obtained in SVC or proximal to area where shunt occurs – Low saturations in LA and LV = R – L shunt – High saturations in RA & RV = L – R shunt
  54. 54. LABORATORY EVALUATION • CARDIAC CATHERIZATION – Determine shunt direction: ratio of pulmonary to systemic blood flow : Qp / Qs – Qp / Qs ratio < 1= R – L shunt – Qp / Qs ratio > 1= L – R shunt
  55. 55. PREMEDICATION a) Omit for infants < six months of age b) Administer under direct supervision of Anesthesiologist in preoperative facility c) Oxygen, ventilation bag, mask and pulse oximetry immediately available d) Oral Premedication • Midazolam 0.25 -1.0 mg/kg • Ketamine 2 - 4 mg/kg • Atropine 0.02 mg/kg
  56. 56. PREMEDICATION e) IV Premedication • Midazolam 0.02 - 0.05 mg/kg titrated in small increments f) IM Premedication • Uncooperative or unable to take orally • Ketamine 1-2 mg/kg • Midazolam 0.2 mg/kg • Glycopyrrolate or Atropine 0.02 mg/kg
  57. 57. MONITORING • Routine CAS monitoring • Precordial or esophageal stethoscope • Continuous airway manometry • Multiple - site temperature measurement • Volumetric urine collection • Pulse oximetry on two different limbs • TEE
  58. 58. MONITORING • PDA – Pulse oximetry right hand to measure pre-ductal oxygenation – 2nd probe on toe to measure post-ductal oxygenation • COARCTATION OF AORTA – Pulse oximeter on right upper limb – Pre and post - coarctation blood pressure cuffs should be placed
  59. 59. ANESTHETIC AGENTS • INHALATIONAL AGENTS – Safe in children with minor cardiac defects – Most common agents used are halothane and sevoflurane in oxygen – Monitor EKG for changes in P wave  retrograde P wave or junctional rhythm may indicate too deep anesthesia
  60. 60. INHALATIONAL ANESTHETICS • HALOTHANE – Depresses myocardial function, alters sinus node function, sensitizes myocardium to catecholamines –  MAP +  HR –  CI +  EF • Relax infundibular spasm in TOF • Agent of choice for HCOM
  61. 61. INHALATIONAL ANESTHETICS SEVOFLURANE • No  HR • Less myocardial depression than Halothane • Mild  SVR → improves systemic flow in L-R shunts • Can produce diastolic dysfunction
  62. 62. INHALATIONAL ANESTHETICS ISOFLURANE • Pungent  not good for induction • Incidence of laryngospasm > 20% • Less myocardial depression than Halothane • Vasodilatation leads to  SVR →  MAP •  HR which can lead to  CI
  63. 63. INHALATIONAL ANESTHETICS DESFLURANE • Pungent  not good for induction; highest incidence of laryngospasm • SNS activation →  with fentanyl •  HR +  SVR • Less myocardial depression than Halothane
  64. 64. INHALATIONAL ANESTHETICS NITROUS OXIDE • Enlarge intravascular air emboli • May cause microbubbles and macrobubbles to expand   obstruction to blood flow in arteries and capillaries • In shunts, potential for bubbles to be shunted into systemic circulation
  65. 65. INHALATIONAL ANESTHETICS NITROUS OXIDE • At 50% concentration does not affect PVR and PAP in children • Mildly  CO at 50% concentration • Avoid in children with limited pulmonary blood flow, PHT or  myocardial function
  66. 66. IM & IV ANESTHETICS KETAMINE • No change in PVR in children when airway maintained & ventilation supported • Sympathomimetic effects help maintain HR, SVR, MAP and contractility • Greater hemodynamic stability in hypovolemic patients • Copious secretions → laryngospasm → atropine or glycopyrrolate
  67. 67. IM & IV ANESTHETICS KETAMINE • Relative contraindications may be coronary insufficiency caused by: – anomalous coronary artery – severe critical AS – hypoplastic left heart syndrome with aortic atresia – hypoplasia of the ascending aorta • Above patients prone to VF d/t coronary insufficiency d/t catecholamine release from ketamine
  68. 68. IM & IV ANESTHETICS IM Induction with Ketamine: • Ketamine 5 mg/kg • Succinylcholine 5 mg/kg or Rocuronium 1.5 – 2.0 mg/kg • Atropine or Glycopyrrolate 0.02 mg/kg IV Induction with Ketamine: • Ketamine 1-2 mg/kg • Succinylcholine 1-2 mg/kg or Rocuronium 0.6-1.2 mg/kg • Atropine or Glycopyrrolate 0.01 mg/kg
  69. 69. IM & IV ANESTHETICS OPIOIDS • Excellent induction agents in very sick children • No cardiodepressant effects if bradycardia avoided • If used with N2O - negative inotropic effects of N2O may appear • Fentanyl 25-100 µg/kg IV • Sufentanil 5-20 µg/kg IV • Pancuronium 0.05 - 0.1 mg/kg IV  offset vagotonic effects of high dose opioids
  70. 70. IM & IV ANESTHETICS ETOMIDATE • CV stability • 0.3 mg/kg IV THIOPENTAL & PROPOFOL • Not recommended in patients with severe cardiac defects • In moderate cardiac defects: – Thiopental 1-2 mg/kg IV or Propofol 1-1.5 mg/kg IV – Patient euvolemic
  71. 71. ANESTHETIC MANAGEMENT • GENERAL PRINCIPLES Where: Q = Blood flow (CO) P = Pressure within a chamber or vessel R = Vascular resistance of pulmonary or systemic vasculature Ability to alter above relationship is the basic tenet of anesthetic management in children with CHD R P Q 
  72. 72. ANESTHETIC MANAGEMENT P  manipulate with positive or negative inotropic agents Q  hydration + preload and inotropes However, the anesthesiologist’s principal focus is an attempt to manipulate resistance, by dilators and constrictors
  73. 73. ANESTHETIC MANAGEMENT • GENERAL CONSIDERATIONS – De-air intravenous lines air bubble in a R-L shunt can cross into systemic circulation and cause a stroke – L-R shunt air bubbles pass into lungs and are absorbed – Endocarditis prophylaxis – Tracheal narrowing d/t subglottic stenosis or associated vascular malformations
  74. 74. ANESTHETIC MANAGEMENT – Tracheal shortening or stenosis esp. in children with trisomy 21 – Strokes from embolic phenomena in R-L shunts and polycythemia – Chronic hypoxemia compensated by polycythemia → ↑ O2 carrying capacity – HCT ≥ 65% → ↑ blood viscosity → tissue hypoxia & ↑ SVR & PVR → venous thrombosis → strokes & cardiac ischemia
  75. 75. ANESTHETIC MANAGEMENT – Normal or low HCT D/T iron deficiency → less deformable RBCs → ↑ blood viscosity – Therefore adequate hydration & decrease RBC mass if HCT > 65% – Diuretics → hypochloremic, hypokalemic metabolic alkalosis
  76. 76. ANESTHETIC MANAGEMENT ANESTHESIA INDUCTION • Myocardial function preserved  IV or inhalational techniques suitable • Severe cardiac defects  IV induction • Modify dosages in patients with severe failure
  77. 77. ANESTHESIC MANAGEMENT ANESTHESIA MAINTENANCE • Depends on preoperative status • Response to induction & tolerance of individual patient • Midazolam 0.15-0.2 mg/IV for amnesia
  78. 78. ANESTHETIC MANAGEMENT • L - R SHUNTS : • Continuous dilution in pulmonary circulation may  onset time of IV agents • Speed of induction with inhalation agents not affected unless CO is significantly reduced • Degree of RV overload and/or failure underappreciated – careful induction
  79. 79. ANESTHETIC MANAGEMENT • L-R SHUNTS : – GOAL =  SVR and ↑ PVR →  L-R shunt • PPV & PEEP increases PVR • Ketamine increases SVR • Inhalation agents decrease SVR
  80. 80. ANESTHETIC MANAGEMENT • R-L SHUNTS : – GOAL : PBF by  SVR and ↓ PVR •  PVR & ↓ SVR → ↓ PBF – Hypoxemia/atelectasis/PEEP – Acidosis/hypercapnia –  HCT – Sympathetic stimulation & surgical stimulation – Vasodilators & inhalation agents → ↓ SVR
  81. 81. ANESTHETIC MANAGEMENT • ↓ PVR &  SVR →  PBF – Hyperoxia/Normal FRC – Alkalosis/hypocapnia – Low HCT – Low mean airway pressure – Blunted stress response – Nitric oxide/ pulmonary vasodilators – Vasoconstrictors & direct manipulation→ SVR
  82. 82. ANESTHETIC MANAGEMENT • R –L SHUNTS : – Continue PE1 infusions – Adequate hydration esp. if HCT > 50% – Inhalation induction prolonged by limited pulmonary blood flow – IV induction times are more rapid d/t bypassing pulmonary circulation dilution – PEEP and PPV increase PVR
  83. 83. ANESTHETIC MANAGEMENT • COMPLEX SHUNTS : • Manipulating PVR or SVR to  PBF will: • Not improve oxygenation • Worsen biventricular failure • Steal circulation from aorta and cause coronary ischemia • Maintain “status” quo with high dose opioids that do not significantly affect heart rate, contractibility, or resistance is recommended
  84. 84. ANESTHETIC MANAGEMENT • COMPLEX SHUNTS : – Short procedures slow gradual induction with low dose Halothane least effect on +ve chronotropy & SVR – Nitrous Oxide limits FiO2 & helps prevent coronary steal & ↓ Halothane requirements
  85. 85. ANESTHETIC MANAGEMENT • OBSTRUCTIVE LESIONS • Lesions with > 50 mmHg pressure gradient + CHF  opioid technique • Optimize preload  improves flow beyond lesion • Avoid tachycardia  ↑ myocardial demand & ↓ flow beyond obstruction • Inhalation agents  -ve inotropy & decrease SVR worsens gradient & flow past obstruction
  86. 86. REGIONAL ANESTHESIA &ANALGESIA • CONSIDERATIONS – Coarctation of aorta  dilated tortuous intercostal collateral arteries   risk for arterial puncture and  absorption of local anesthetic during intercostal blockade – Lungs may absorb up to 80% of local anesthetic on first passage. Therefore  risk of local anesthetic toxicity in R-L shunts
  87. 87. • Central axis blockade may cause vasodilation which can: i. Be hazardous in patients with significant AS or left-sided obstructive lesions ii. Cause  oxyhemoglobin saturation in R-L shunts iii. Improve microcirculation flow and  venous thrombosis in patients with polycythemia • Children with chronic cyanosis are at risk for coagulation abnormalities REGIONAL ANESTHESIA &ANALGESIA
  88. 88. POSTOPERATIVE MANAGEMENT • Children with CHD are very susceptible to: i. Deleterious effects of hypoventilation ii. Mild decreases in oxyhemoglobin saturation Therefore, give supplemental O2 and maintain patent airway • In patients with single ventricle titrate SaO2 to 85%. Higher oxygen saturations can  PVR  PBF   systemic blood flow
  89. 89. • Pain   catecholamines which can affect vascular resistance and shunt direction • Anticipate conduction disturbances in septal defects • Pain  infundibular spasm in TOF  RVOT obstruction  cyanosis, hypoxia, syncope, seizures, acidosis and death POSTOPERATIVE MANAGEMENT

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