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Anaesthesia for closed heart procedures   pda & coa
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Anaesthesia for closed heart procedures pda & coa



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  • 3. LESIONS CORRECTED WITH CLOSEDPROCEDURES Patentductus arteriousus Co-arctation of aorta
  • 4. CLOSED PALLIATIVE PROCEDURES o PA Banding o Blalock - Taussig shunt o Balloon atrial septostomies (Rashkind Procedures)
  • 5. PATENT DUCTUS ARTERIOUSUS1 in 2500live , full term births 10 % of all congenital heart defects Girls are affected twice than boys Prenatal exposure to rubella virus during first trimester of pregnancy
  • 6. ANATOMY PDA extends from the post. Descending aorta near the origin of left sub clavian artery to the anterior surface of the main pulmonary artery It is the remnant of sixth branchial arch A bilateral PDA is possible
  • 7. STRUCTURAL DIFFERENCE BETWEENPDA& AORTA + PULMONARY ARTERY Aorta & pulmonary artery`s internal media is composed of elastic fibers Internal media of PDA is composed of smooth muscle in both longitudinal & circumferential arrangements  The muscle constrict when exposed to increased Pao2  This response becomes more dramatic as the fetus matures
  • 8. PATHOPHYSIOLOGY In the fetus blood flow from the RV is diverted from the high resistance pulmonary bed via the ductus to the descending aorta Hemodynamics of a PDA is similar to VSD- left to right shunt flow is determind by the capacity of the ductus to impede flow from the aorta to the PA If the ductus is large,stunted blood flow is determined by the pulm. Vasculature resistance to systemic vascular resistance
  • 9. NATURAL COURSEo Functional closure of ductus is due to vas o Constriction after termo Anatomic closure is due to intimal proliferation and fibrosis which is complete at one month
  • 10. CATEGORIZATION OF PDA Done on the degree of left to right shunt,which is determined by both the size and the length of the duct and the diff. bet. the SVR and PVR  SILENT: tiny PDA detected by echocardiography  SMALL: continuous murmer common;Qp/Qs of 1.5to2.2:1  MODERATE: continous murmer present;Qp/Qs>2.2:1  EISSNMENGER:continous murmer absent;substantial pulm.HT,differential hypoxemia;and differential cyanosis(pink fingers,blue toes)
  • 11. DIAGNOSIS Signs  tachypnea  diaphoresis  decreased exercise tolerance  failure to thrive  recurrent respiratory infection  lobar emphysema / collapse  cardiac failure  cardiac enlargement  bacterial endocarditis  irreversible pulmonary vascular disease
  • 12. PHYSICAL EXAMINATION continuous machine murmur which gets louder through out systole with a peak at the 2nd heart sound & gets softer through out diastole Murmur is loudest at 1st or 2nd inter costal space at left sternal border Pulse pressure- wide- prominent or bounding pulse Pulse biferiens-two distinct peaks seprated by a deep cleft, noted on the intra-arterial wave form is a specific & sensitive indicator of PDA with Left to right shunting in the neonate ECG- usually normalwith large L-R flow- LVH or Lt arterial enlargement
  • 13. o RVH- if PDA has caused pulmonary occlusive disease o Chest x-ray o small PDA – normal X-ray o as flow increases- prominent pulmonary -prominent aortic knob o further increase in flow - left heart enlargement - increase in pulmonary vascular marking ( indicative of failure)o Echocardiographyo main diagnostic procedure for PDAo 2D Echo- can identify the aortic end of the ductuso Continuous wave Doppler – can detect abnormal flow in PAo Color flow Doppler- can visualize the jet of abnormal flow & determine more information about the size and shape of the ductus
  • 14. INDICATION FOR INTERVENTION Unnecessary in an asymptomatic infant with a small left to right shunt Necessary for those who have signs of a significant ductal left –to- right shunt during the course of the respiratory distress syndrome Surgical ligation is required in the infants who are unresponsive to Indomethacin
  • 15. C.I TO DUCTAL CLOSURE Irreversible pulmonary HT Active endarteritis
  • 16. PREOPERATIVE PREPARATION Prophylactic antibiotics Vit. K (preterm infants)
  • 17. INTRA-OPERATIVE MONITERING ECGB .P – invasive Capnography Pulse oximeter (two) – Rt hand & one on lower extrimity Temperature monitering Esophageal stethoscope – to listen to murmur
  • 18. PREMEDICATION Usually not recquired ORAL PREMEDICANT COMBINATIONS Mepridine – 1.5 mg/kg(max. 100mg) Atropine -0.02mg/kg(max.0.4mg) Diazepam 0.15mg/kg(10mg) or Mepridine – 2- 3mg/kg(max.100 mg) Diazepam -0.1 mg/kg(max.10mg) Fentanyl(oral/transmucosal) – 15 – 20 micro gram/kg or Midazolam -0.5 – 0.75 mg/kg(max.5mg) INTRAMUSCULAR PREMIDICANT COMBINATIONS Morphine 0.2 mg /kg(max.10mg) oro Midazolam -0.08mg/kg(max5mg) (recommended for children over 1 year of age)
  • 19. INDUCTION Fentanyl – 2microg/kg body wt. Sleep dose of thiopentone Succinyl choline – 1mg/kg Ventilation Larynx sprayed with 2% ligocaine Maintenance with N2O & O2 mixture( 60:40) Halothane and non depolarising agents Other supplemental drugs used are ketamine,isoflurane and midazolam
  • 20. MAINTENANCE N2O +O2+ Halothane + non depolarising agents Sodium Nitropruside – 1 vial in 5% of 500 ml of dextrose in micro drip set started when the ductus is dissected out and the systolic pressure is brought down to 60 mm Hg Once the ligation is complete the SNP is stopped and continued if the pressure rises post - operatively
  • 21. FOLL. LIGATION OF PDA Diastolic pressure rises in the typical PDA pt. In selected pt`s – PA pressure monitoring m/b carried out In typical PDA pt`s with no change in PA pressure after occlusion If PA pressure falls in pt`s with pulmonary HT, then the degree of increased resistance is minimal & the ductus m/b ligated safely If PA pressure increases with severe pulmonary HT – then ligation carries a high mortality
  • 22. ON THE CLOSURE OFDUCTUS The diastolic component of the murmur will disappear Systolic component persist but without significance
  • 23. SERIOUS COMPLICATION A serious complication is increased PVR with severe Pulmonary hypertension- reversal of flow –RHF If ligation of the ductus is performed at this stage • death may occur promptly owing to the closure of the escape route of the pulmonary circuito Damage to the laryngeal nerve
  • 24. INTERVENTIONAL TECHNIQUES TRANSCATHTER TREATMENT -for ducts smaller than 8mm have been establised SURGICAL TREATMENT -either by ligation or by putting clips -greater morbidity and mortality -immediate closure in more than 95%of patients -surgical mortality in adults is 1%to 3.5% and is due to pulmonary art. Hypertension and difficult ductal morphology -reserved for those in whom PDA is too large for device closure VIDEO ASSISTED THORACOSCOPIC SURGERY -costly -experience is required
  • 25. CO –ARCTATION OF AORTA Etiology and risk of occurrence -1 in 2000 live births Sixth most common congenital heart disease Narrowing of aortic lumen from protrusion from within posterior and lateral aortic media Mortality is associated with - cardiac failure (25%) -Aortic rupture(21%) -Endocarditis (18%) -Cerebrovascular hemorrhage(11.5%) -Others –HT -CAD
  • 26. ANATOMY Classificationof co-arctation is based on the relationship with the ductus arteriosus Preductal – proximal to the ductus , infantile type Postductal – distal to the fibrosed ductus,adult type
  • 28. SEGMENTS OF THE AORTA Ascending aorta to innominate to artery proximal arch from innominate to left carotid Distal arch from left carotid to left subclavian artery Isthmus from left subclavian to co –arctation Aorta at the level of the diaphragm
  • 29. PRE – DUCTAL CO ARC TATION Morphology -Localised shellf in the postero lateral aortic wall opposite the ductus More assoc. with neonates CLINICAL FEATURES More in males Associated with –gonadal dysgenesis (Turner syndrome -Biscuspid aortic valve -VSD -MS/MR
  • 30. NEONATES Left ventricular failure –  increase in left ventricular wall stress after closure of arterial duct  Systemic hypo perfusion  Left to right shunting across patent foramen ovale (PFO) and pulmonary venous hyper tension secondary to heart failure cause pulmonary arterial hypertension  Peripheral pulse are weak  If L.V function is improved with medical management, a significant pressure difference then develops between the arms & the legs, allowing detection of a pulse discrepancy
  • 31. LAB INVESTIGATION ECG –RAD &RVH Chest x- ray  Cardiomeagaly  pulmonary arterial & venous engorgement  Echocardiography  Demonstrates the posterior shelf & the degree of associated isthmic or transverse arch hyopoplasia Doppler echo cardiography -is helpful if ductus is closed - it demonstrates a high velocity jet during systole & diastole
  • 32. MANAGEMENT Prostaglandin therapy  PGE1 infusion to dilate the ductus arteriosus, the pressure difference may be obliterated across the site of co-arctation because the fetal flow pattern is re- established  This also improves the renal perfusion, which in turn reverses the associated metabolic acidosis
  • 33. INTERVENTION Surgical- excision of the area of co-arctation and extended end to end repair or end to side anastomosis with absorbable sutures to allow remodeling of the aorta with time Subclavian flap aortoplasty-  Less popular now days Balloon dialation – does not have in management in this age group Early surgery – lower incidence of long term hypertension
  • 34. INFANTS & CHILDRENPRESENTATION Reduced femoral pulses Hypertension Heart failure is uncommon because, the L.V has a chance to become hypertrophied Complaints of headache, cold extremities and claudication with exercise is noted in older child & adolescent age group Midsystolic murmur over the anterior chest, back is most frequent
  • 35.  Lab investigation ECG -LVH with co-existing RVHo CHEST-X RAY  pre –stenotic & post stenotic dilatation of the proximal descending thoracic aorta  Rib notching – unilateral or bilateral in 50% of case ECHO cardiography - Demonstrates a post. Shelf -A well expanded isthmus and trasverse aortic arch -High velocity continuous jet through the co- arctation site
  • 36. INTERVENTION Balloon dilation Surgery reserved for arch hypoplasia  Extended end to end anastomosis is the currently favored surgical approach with patch augmentation
  • 37. COMPLICATIONS Paradoxical HT in immediate post. Op ( not seen with balloon dilation ) Becoz of HT – cerebral aneurysm & hemorrage  Hypertensive encephalopathy  Rupture of aorta  LVF  Infective endocarditis
  • 38. ADULT PRESENTATION Presents with simple co-arctation Associated anomalies –  bicuspid aortic valve(80 %)  Intracranial aneurysms (2-10%)
  • 39. CLINICAL FEATURES Asymptomatic Epistaxis Headache Leg weakness on exertionC H F Angina Aortic stenosis Aortic dissection Un explained intracerebral hemorrhage Leg claudication ( pain)
  • 40. CLINICAL EXAMINATION Upper limb HT Differential systolic blood pressure of atleast 10mm Hg(brachial>popliteal) Radial-femoral pulse delay Auscultation- interscapular systolic murmur Fundoscopic examination-corkscrew tortuosity of retinal arterioles
  • 41. INTERVENTION Surgical Balloon dilatation
  • 42. ANAESTHETIC MANAGEMENT PRE-OP PREPARATION  Prophylatic antibiotics  Control of BP  BETA-blockers o Intra Operative Monitoring Invasive arterial pressure monitoring in right radial artery and femoral artery o CVP Monitoring o Capnography o Pulse Oximitry o Spinal Cord Monitoring -
  • 43. ANAESTHETIC INDUCTION G.A with controlled ventilation is the technique of choice Epidural anaesthesia avoided as it may mask paraplegia Total IV Anaesthesia with opiates is useful in neonates with cardiac failure or cardiovascular instabilty Avoid ketamine Isoflurane preffered becoz of its effect on afterload
  • 44. MAINTENANCE Monitor lower body pressure closely-pressure should not fall 45mmHg Provide analgesia for intra&postop Epidural analgesia technique+/-; Intercostal nerve blocks not recommended becoz of collaterals Volatile agents make blood pressure control easy Start antihypertensive control early after cross clamp has been removed,using beta – blockade,then nitroprusside
  • 45. THANK YOU