Patent ductus arteriosus and anesthesia

1. PATENT DUCTUS
ARTERIOSUS
MODERATOR :Dr.Prashant
PRESENTER: Dr. Richa

2. INTRODUCTION
 FETAL CIRCULATION:
SPO2 = 40%
Po2=12-14mmHg
SPO2 =80%
Po2=32-35mmHg
SPO2 =70%
Po2=28-30%
SPO2 =55-60%
Po2=20-22
SPO2 =65
Po2=26-28

3.  Normal transition of circulation after birth:

5. AT birth….
 Placenta removed  portal blood pressure falls  DV closes
 Blood is oxygenated in lungs  DA exposed to oxygenated blood VC
 First breath Pulmonary vascular resistance decreases now
SVR>PVR  LAP> RAP  closure of foramen ovale

6. • Although closure of DA occurs primarily by increased oxygen tension,
successful complete closure requires arterial muscular tissue.
• DA begins to close within first 24 hours after delivery
• Completed sealed off in FIRST MONTH
• During this critical period, infant can readily revert from adult
circulation to fetal circulation (FLIP-FLOP CIRCULATION)
• If shunt persists (preterm babies/maternal rubella) it leads to
shunting of blood from left right (ACYANOTIC CHD)

7.  Diagnosis of persistent fetal circulation can be confirmed
by measuring PaO2 in blood samples obtained
simultaneously from preductal (right radial) and
postductal (umblical, posterior tibial or dorsalis pedis)
arteries
 The presence of PaO2 differences of > 20 mmHg confirms
the diagnosis

8. ANATOMY
DA has diameter of 5-15mm
Length of 2-15mm
Relations:
Posteriorly: left main bronchus
Anteriorly: Vagus nerve
Recurrent laryngeal nerve encircles ductus and ascends into neck

9.  During fetal development ductus arteriosus connects the
left pulmonary artery and descending aorta
 Distal to left subclavian artery.
 Right  left shunt in fetus(PVR>SVR) , bypassing the lungs
 F:M = 2:1

10. ASSOCIATED ANOMALIES
 EXTRACARDIAC
 Mental retardation
 Eye defects
 Deafness
 Sternal deformities
 Scoliosis
 clubfoot

11.  CARDIAC
 PULMONARY ATRESIA, PULMONARY STENOSIS, TRICUSPID ATRESIA
 SYNDROMES
 CHARGE
 EDWARD
 PATAUS
 GOLDENHAR : oculoauriculovertebral dysplasia or hemifacial microsomia
 VATER: vertebral, anal, TEF, renal anomalies

12. RUBELLA SYNDROME

13. DUCTUS DEPENDENT CARDIAC LESIONS
Lesions restricting
pulmonary blood flow
• PULMONARY ATRESIA
• TRICUSPID ATRESIA
LESIONS RESTRICTING
SYSTEMIC BLOOD FLOW
• MS WITH ASD
• AS with ASD
• PREDUCTAL COA
• HYPOPLASTIC LEFT
HEART SYNDROME

14. CLOSURE OF DA
 The patency of PDA in fetal life is due to:
 low fetal oxygen tension and
 cyclooxygenase mediated products of arachidonic
acid metabolism= PGE2 & PGI2 VD of DA
 High levels of PGE2 & PGI2 are due :
 Production by placenta
 Decreased metabolism by fetal lungs

15.  At birth : abrupt increase in oxygen tension inhibits ductal
smooth muscle potassium channels  calcium influx VC
 PGE2 & PGI2 levels falls due to their metabolism in lungs
and decreased source of production (placenta removed)
 Functional closure : 24-48 hours
 Permanent closure within one month

16. INCIDENCE AND PATHOPHYSIOLOGY
 50% infants weighing <1000gm
 20.2% infants weighing <1750 gm have hemodynamically
significant PDA
 In term infants, DA closes soon after birth in response to
increased oxygen arterial tension
 In preterm infants, it has thinner and poorly contractile
muscular layer with diminished response to increasing O2

17.  Additionally , preterm infants often suffer hypoxemia due
to RDS (not much stimulus for closure)
 Ultimately, preterm have both reduced stimulus to and
reduced response to physiologic closure.

18. Large
size PDA
• Magnitude of shunting depends
on resistance to flow through
the DA
L R
shunt
Aortic
pressure
transmitted to
pulmonary
trunk
• Increased pulmonary
circulation results in
decreased lung complaince
and increased work of
breathing
• Pulmonary edema
More to left PA
due to close
relationship of
PDA
Pulmonary
HTN, RVH

19. L R shunt
Increased
cardiac work to
increase stroke
volume and HR
LVH
Subendocardial
ischemia due to
O2 D:S
mismatch
Decreased
systemic blood
flow
Increased
pulmonary
blood flow
Volume
overload on left
side of heart

20. Long standing
PHTN, RVH
• PA pressure >
25mmHg at
rest
• Or > 30 mmHg
with exercise
Muscular
hypertrophy,
internal fibrosis
and increased
pulm. VR
Reversal of shunt • EISENMENGER SYNDROME

21.  Pulmonary hypertension can present as:
 DYNAMIC: related to shunt flows that respond to reduction of the
shunt
 REACTIVE: difficult variety, it is challenging to control in
perioperative period
 SHUNT REVERSAL  Eisenmenger physiology ( central cyanosis,
dyspnea, fatigue, hemoptysis, syncope and right sided heart
failure)

22.  The amount of shunting depends on :
 size of ductus
 pressure difference between aorta and pulmonary
artery and
 ratio between pulmonary and systemic vascular
resistance

24. HISTORY OF BABY WITH PDA
 Irritability ,feed poorly, failure to gain weight and sweat excessively
 Increased respiratory effort and rate (breathlessness)
 Prone to develop recurrent URTI and pneumonia
 Poor growth
 Easy fatiguability

25.  H/O associated anomalies
 Drug history
 History of previous cardiac/other surgeries

26. EXAMINATION
 Tachycardia
 Increased respiratory rate
 Physical underdevelopment
 Wide pulse pressure- bounding peripheral pulses
 SYSTOLIC hypertension and low diastolic pressure
 On I & P: Hyperkinetic apex, continuous thrill in 2nd ICS

27.  Accentuated S1 or normal
 S2 narrow split or paradoxical split= masked by murmur
 continuous murmur (machinery murmur) **= upper left
sternal border, radiating down the sternal border and into
back
 GRAHAM steel murmur in Eisenmenger syndrome
 Differential cyanosis and clubbing in shunt reversal

28.  S/S of congestive heart failure: failure to thrive, cough
dyspnea, tachypnea, tachycardia, hepatosplenomegaly

30. INVESTIGATIONS
 CBC
 Electrolytes
 Coagulation profile
 Platelet count
 Serum proteins
 Calcium levels
 Arterial blood gas
 Urine analysis
 CXR
 ECG: sinus tachycardia , AF
 ECHO= doppler/ M-mode

31. CXR

32.  DOPPLER ECHO : for confirmation of diagnosis
 COLOR DOPPLER: can visualise jet of abnormal flow
 M-MODE ECHO :
 Measure cardiac chambers= LA ,LV enlarged in
moderate to large PDA
 Quantify LV and RV systolic function

33. COMPLICATIONS OF PDA
 CHF: moderate to large PDA due to pulm. overcirculation
and left heart volume overload
 Atrial flutter and AF
 Hypertensive pulmonary vascular disease
 Endarteritis
 Anneurysm of DA
 Dissection/ rupture of DA: rarely

34. ASSESSMENT OF SEVERITY
 Heart size
 Diastolic murmur
 Pulse pressure

35. MANAGEMENT OF PDA

36. Medical management
 Patients with congestive cardiac failure:
 Fluid restriction
 Furosemide
 Dopamine
 Digitalis is not used in small preterm infants because it does not
effectively improve stroke volume or ventricular emptying,
 It decreases HR detrimental decrease in C.O.
 Furthermore , digitalis toxicity increases mortality in preterm
infants.

37.  Role of prostaglandins: PGE1 used to keep ductus patent in duct
dependent lesions
 Ibuprofen, indomethacin is used for closure of duct
 Indomethacin inhibits cyclooxygenase decreased production of
Pg
 Dose : 0.1-0.2mg/kg 3 doses in every 12 hours closes duct within
24 hours
 A/E: mesenteric,renal and cerebral blood flow decreased

38.  Anti-arrythmic drugs
 Vasodilators : PGI2, CCB, endothelin antagonist and PDE
inhibitors
 Other drugs : Diuretics and digoxin (avoided in preterm)

39. Minimally invasive technique
 Transcatheter closure with intravascular coils for small
PDA
 Catheter introduced sacs or umbrella like device in
moderate to large PDA

40. SURGICAL CLOSURE
 Division or ligation of PDA via left thoractomy
 Thoracoscopic technique : less pain, faster recovery
compared to thoracotomy

41. ANESTHESIA CONSIDERATIONS
 Avoid
 Hypothermia
 Hemodilution
 Hypoxia
 Hyperoxia
 Cross matched blood
 Left thoracotomy approach is used :position
 Postoperative ventilation

42.  Anesthesia drugs cause changes in SVR and PVR resulting
in unbalancing of PBF
 High PBF leads to pulmonary edema and desaturation
 Lower PBF leads to desaturation and acidosis

44. Preoperative preparation
 Informed consent
 Hydration
 Avoid fluid overload
 Inotropic support if required
 Good preoperative medication is important to reduce anxiety and
smooth induction
 Pulse oximetery is monitored after giving premedication
 CHOICES of drugs: midazolam 0.5mg/kg oral, 0.05-0.2mg/kg IV (may
not be required in neonate)

45. INDUCTION
 Preoxygenation
 Prolonged onset time of IV agents is expected due to L R
shunt
 No change in inhalational induction
 IV agents : Ketamine 1-2mg/kg with glycopyrrolate 20mcg/kg
 NMBA : vecuronium 0.1 mg/kg IV
 If no IV line: sevoflurane induction
 SUCCINYLVCHOLINE avoided (contracture of PDA)

46.  Dexamethasone 0.2-0.5mg/kg
 Ondansetron 0.1mg/kg to avoid nausea and vomiting

47. MONITORING
 ECG
 Pulse oximetery in right hand
 Invasive BP in right side
 etCO2
 Airway pressure
 Temperature monitoring
 ABG
 TEE
 Temperature
 Urine output

48. MAINTENANCE
 Sevoflurane+ air+ Oxygen
 Vecuronium
 Fentanyl (small doses) 1-2 mcg/kg to blunt hemodynamic changes during
stimuli
 Increase in Oxygen concentration decreases PVR
 NITROUS OXIDE IS AVOIDED (pulmonary HTN)
 Prevention of hypothermia

50. HEMODYNAMICS
 Fluid therapy: isotonic fluids with BSL monitoring / 1-2.5%
dextrose with BSS
 Maintenance fluid 4ml/kg/hr
 IV tubing should be bubble free to prevent embolization
 Hematocrit is maintained as hemodilution leads to
increase in L R shunt
 Blood loss is replaced with PRBC / 1:3 crytalloid,
mainaining Hct >30%

51.  Bradycardia is watched for while handing PDA (RLN
vagus nerve)
 Systolic hypotension may occur at time of ligation of DA
 Increase in DBP abruptly may occur after ligation of duct
 This is due to elimination of PVR from circulation

52. VENTILATION
 Controlled
 Ventilatory goals: TV adjusted to keep PIP pressure between 15
to 25 cm Hg
 Fi02 adjusted to keep PaO2 between 50-70 mmHg
 SPo2 between 87% to 92% ( to avoid ROP in neonates)
 etCO2 30-35cm H2O
 Hypoventilation can reverse the shunt due to HPV
 Hyperventilation can increase L R shunt due to reduction in
pulmonary vascular resistance

53.  Paracetamol and local infilteration adequate for postprocedural
analgesia
 Nephrotoxic drugs are avoided as iodinated contrast given during
procedure cause renal dysfunction and predisposes to
nephrotoxicity
 Postoperative ventilation needed in preterm /premature babies

54. OTHER CONCERNS
 Blood loss if control of PDA is lost during ligation
 Hypoglycemia is frequent complication in neonates
 Hypothermia : preterm neonates have impaired
thermoregulation
 Systemic hypertension in postoperative period Mx SNP

55. INTRAOPERATIVE COMPLICATIONS
 Tear/ avulsion of DA with profuse bleeding
 Bradycardia
 Inadvertent left pulmonary artery/aortic ligation
 Phrenic nerve injury
 Recurrent laryngeal nerve injury
 Trauma to thoracic duct
 Residual shunt
 Postoperative aneurysm
 Postoperative hypertension *
 Bacterial endocarditis

57. THANKYOU !!