Cardiac emergencies or screening in neonate.pptx

approach to cardiac emergencies in neonate

1. SCREENING OF CONGENITAL HEART DISEASE Dr Manish Chokhandre Consultant Pediatric Cardiologist Swasthyam Superspeciality Hospital, Nagpur

2. Introduction Cardiac Defects- most stressful situation/emergencies in ER Often complex Coexisting pathology-heart lung interaction High mortality Early diagnosis and management –Key

3. Major cardiac defects

4. Major Neonatal Cardiac Emergencies Blue Baby Grey Baby Pink Baby Cyanosis Shock Heart Failure Arrhythmias HR issue Duct dependent Pulmonary circ Duct dependent Syatemic circ Left to right shunt Septicemia , respiratory disorders, persistent pulmonary hypertension of newborn, (PPHN),inborn errors of metabolism and so on

5. 5 BASIC QUESTIONS TO BE ANSWERED… 1. Is it a CHD?? 2. If yes: Cyanotic or acyanotic ?? 3. Pulmonary Blood flow: Increased? 4. PAH: +/-?? 5. Duct dependent lesion??

6. 2 nd question: Cyanotic or acyanotic Clinically: nail beds/lips/tongue blue But if saturation between 85-93% the human eye cannot detect cyanosis So, the gold standard of detection of cyanosis is PULSE OXIMETER Infact the pulse-ox is called the 5 TH VITAL SIGN

7. Classification of chd Acyanotic Increase PBF ASD VSD PDA AP window Combined Normal PBF AS/PS Cyanotic Decrease PBF TOF Pulm Atresia Increase PBF TGA TAPVC Truncus arteriosus Pulse-oximeter

8. Duct dependent circulation

9. Cyanotic CHD

10. Cyanotic CHD with increased pulmonary blood flow- TGA Assist "Mixing” Prostaglandin E1 Atrial Septostomy – usually not urgent Manage pulmonary edema Diuresis Optimize lung recruitment and gas exchange Avoid excess FiO 2 and hyperventilation Optimize systemic output Optimize preload/inotropic support Optimize hemoglobin

11. Cyanotic Decrease PBF TOF Pulm Atresia Increase PBF TGA TAPVC Truncus arteriosus

12. Objective way to determine PBF- CXR

13. Truncus

14. TAPVC

15. TOF-PA

16. Case-2 D3 old baby –suddenly sick • Poor feeding , Not passing urine • Colour not Looking good –pale • Cold peripheries ,Tachypnoea , tachycardia • poor pulses ,BP 32/20, metabolic acidosis ,raised lactates Shock

17. Case-2 Ventilated • Fluid challenge  oliguria  unresponsive • Inotropes  high doses  hypotension persists • Non cardiac- Sepsis ???

18. Labs WBC 21, Hct 41 AST 360, ALT 350 BUN 65, Cr 1.2 Pre/Post-ductal Sats (100% NRB) RUE 99% LLE 99%   ABG (Rt radial artery, FiO2 1.0) 6.92/24/170/Lactate 9.5 Case 2 Additional Data

19. DD-Shock, metabolic acidosis Sepsis Sepsis Sepsis Congenital Heart Disease Ductal-dependent systemic blood flow Critical Coarctation of the aorta Interrupted aortic arch Critical Aortic Stenosis Hypoplastic Left Heart Syndrome

20. Major Neonatal Cardiac Emergencies Blue Baby Grey Baby Pink Baby Cyanosis Shock Heart Failure Arrhythmias HR issue Duct dependent Pulmonary circ Duct dependent Syatemic circ Left to right shunt Septicemia , respiratory disorders, persistent pulmonary hypertension of newborn, (PPHN),inborn errors of metabolism and so on

21. Differential Diagnosis – Shock/Metabolic acidosis Less than 1 months old Congenital Heart Disease Ductal-dependent systemic blood flow Critical Coarctation of the aorta Interrupted aortic arch Critical Aortic Stenosis Hypoplastic Left Heart Syndrome Sepsis Inborn Error of metabolism

22. Hallmark presentation: acute shock with severe progressive metabolic acidosis End-organ injury common Fetal diagnosis has decreased incidence 4-Ext BP discrepancy – essential part of workup for HTN in children Cannot rule out CoA in setting of open PDA on ECHO Left sided obstructive lesions

23. PDA dependent systemic circulation: Clinical presentation and clinical clues A healthy newborn who presents after 48-72 hrs of life with sudden onset of pallor, grey appearance and breathing difficulty. Not passing urine and not taking feeds Metabolic acidosis Clinical clues- Harsh systolic murmur- Obstructive lesions Differential cyanosis Differential pulse

24. Duct dependent systemic circulation: Initial management Early diagnosis / rapid intervention Restore systemic blood flow Prostaglandin E1 Inotropic support Afterload reduction contraindicated - reduce coronary perfusion Mechanical ventilation/respiratory support Eliminate work of breathing Lung recruitment After restoration of systemic blood flow Diuresis If L-R shunt, manipulate SVR/PVR to limit pulmonary flow

25. PGE1 When to use How to give Dosage and monitoring

26. How to give? Dose - 0.001-0.4 microgram/kg/min infusion Higher doses 0.1 mic/kg/min should be used to reopen the closed PDA (or if there is sudden onset of severe cyanosis or shock). Increments of 0.05 microgram /kg/min every 5-10 minutes Run continuously in separate IV line D5,D10,NS, not with meds Once the response, dose can be reduced to a minimum Response: Improved PaO2 or BP , Improvement of peripheral perfusion, tissue oxygenation and metabolic acidosis

27. Preparation 500 microgram per vial, dilute it in 50 ml of 5 % dextrose and start in infusion pump. 3×wt×microgram/kg/min divided by concentration (mg) in 50 ml = flow rate in ml/ hr So for wt of 3 kg child and dose of 0.1mic/kg/min • 3x3x0.1/0.5=ml/hr ( 0.9/0.5) = 1.8 ml per hr infusion will give you 0.1 microgram/kg/min.

28. Probability of prostaglandin sensitive lesion is increased In cyanosed neonate - failed hyperoxia test + murmur In a non -cyanosed neonate - abnormal pulses Whenever in doubt, Start PGE1 , though may not be effective in certain lesions

29. Duct dependent lesion Shock, acidosis Central caynosis History/Exam oligemia Plethora Plethora Systemic pulmonary Coarctation HLHS Critical AS Arch interruption CXR TOF Tri Atresia PA/IVS DORV/PA/PS Critical PS Ebstein’s PA TGA Truncus TAPVC

30. Major Neonatal Cardiac Emergencies Blue Baby Grey Baby Pink Baby Cyanosis Shock Heart Failure Arrhythmias HR issue Duct dependent Pulmonary circ Duct dependent Syatemic circ Left to right shunt Septicemia , respiratory disorders, persistent pulmonary hypertension of newborn, (PPHN),inborn errors of metabolism and so on

31. Classical Left to right shunt with HF Preterm with significant post tricuspid shunt lesions (e.g. VSD ,PDA ,Aorto- Pulmonary window) Severe valvular regurgitant lesions (e.g. Mitral regurgitation associated with AV canal defects) Anomalous Left Coronary Artery from Pulmonary Artery(ALCAPA) Cardiomyopathy

32. Presentation Feeding intolerance Weight loss/poor weight gain Respiratory distress Pulmonary oedema Need of Respiratory support O2 requirement Hyperdynamic circulation CXR-Cardiomegaly and plethora

33. Preterm PDA Steal phenomenon like cerebral steal (manifesting as apnea) or steal from gut (manifesting as necrotizing enterocolitis ). Bounding pulses along with wide pulse pressure should give a suspicion After surfactant therapy, they show improvement and ventilatory requirements go down . As Hyaline membrane disease improves and PVR falls, PDA shunt becomes significant and ventilatory requirements become higher again

34. Management   If needs bolus, give 5-10 mL/kg and titrate. Continuous reassessment. Never wrong to think sepsis and treat as such – but ALWAYS reassess therapy if patient doesn’t respond appropriately. Avoid cardiac depressant drugs —Benzo’s, Propofol. EKG, continuous monitoring for arrhythmias QTc, ST changes, Ventricular or atrial enlargement. Ectopy worrisome . CAREFUL WITH INTUBATION !! Once intubated usually more stable but arrest can/does occur peri-intubation.

35. Adjust oral therapy Volume,Ionotropes Diuretics Vasodilators Ultrafiltration Ionotropes Diuretics Vasodilators Vasopressors Ventilation

36. What inotropic agents would you initiate? A: Epinephrine B: Milrinone C: Dobutamine D: Dopamine E: Nitroprusside F: Other Acute heart failure-Management decisions Hypertension

37. AHF How would you determine the need to increase or decrease inotropic support in this patient? Clinical assessment of end-organ function (UOP, BUN/Cr ratio, LFTs, physical exam) Echo assessment of ventricular function Serial lactate measurements Serial BNP measurements Goal oriented therapy with SVC oximetry (surrogate mixed-venous Sat)

38. Definitive therapy All hemodynamically significant shunts/defects should be closed -Pharmacologic therapy in preterm Neonates - PDA -Device closure or surgery (VSD/AP window, ALCAPA, Valve repair)

39. Major Neonatal Cardiac Emergencies Blue Baby Grey Baby Pink Baby Cyanosis Shock Heart Failure Arrhythmias HR issue Duct dependent Pulmonary circ Duct dependent Syatemic circ Left to right shunt Septicemia , respiratory disorders, persistent pulmonary hypertension of newborn, (PPHN),inborn errors of metabolism and so on

40. ARRHYTHMIA

41. Arrhythmia Tachyarrhythmia Narrow complex QRS<90ms Unstable Cardioversion Stable Adenosine Amiodarone Wide complex QRS>90ms Unstable C ardioversion Stable Amiodarone Bradyarrhythmia CHB pacemaker Pulseless NALS

42. Summary Neonatal cardiac emergencies: life-threatening Ductus‑dependent lesions – Main cause Acutely ill neonate- High index of suspicion for CHD History/Physical exam/ hyperoxia test/ pulse discrepancy/ CXR- ongoing emergency management Timely intervention is life saving

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