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The Crashing Cardiac Baby

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The Crashing Cardiac Baby

  1. 1. The ashing Cr c Baby Cardia Looks Sick @! This Kid Or: Holy $# Dan Park MUSC Pediatric cy Medicine Emergen
  2. 2. You only retain 10% of a 1 hr lecture after 3 weeks (Bligh 2000) heard somewhere high estimate want to hit the most high yield practical information for you if you take away 10% i’ll be pumped
  3. 3. Pediatric Cardiac Emergencies Kawasaki disease Arrhythmias Congenital heart disease Congestive Myocarditis heart Infective failure Corrected endocarditis congenital heart disease Hypertrophic Heart transplant cardiomyopathy broad topic why i chose it: super interesting, scares the shit out of me teaching it makes me understand it better
  4. 4. 60 combined years of pediatric ER experience hypoplastic left heart coarctation of aorta post surgical Unstable SVT coarctation of aorta coarctation of aorta V fib Unstable SVT V fib single ventricle coarctation of aorta asked most experienced ER attendings how many times they’ve taken care of a crashing cardiac kid this works out to about once every 5 years that’s not nothing, but it happens rarely enough that we might start to forget stuff
  5. 5. when you overestimate the probability of events associated with memorable or vivid occurrences or underestimate things you haven’t For the nerds: seen in a while It impacts your PRETEST PROBABILITY ilit ilab Ava ias yB common trick that your mind plays on you that can lead to misdiagnosis or error its the tendency to judge probabilities based on how easily examples come to mind you don’t see crashing cardiac kids often so your mind doesn’t even consider them as a possibility when you see a sick kid
  6. 6. Most of the kids that come through the peds side are healthy and will do fine no matter what you do Your real job is to find the needle in the haystack. This is also called Ruling out the worst case scenario. The whole point of spending time in the peds ER is to see a shit ton of healthy kids so you know what a sick one looks like when you see one
  7. 7. CASE 7 day old boy is brought to the ED by his frantic father. He reports that his son was having difficulty feeding throughout the day and then became limp in his arms just before presentation. On exam, you note a cyanotic infant with the following vital signs: T 37. C, HR 165, RR 65 (labored), and BP 72/palp. The patient is poorly perfused and the pulse oximetry reading is not detectable. The intervention most likely to benefit this child is a: a. Stat chest xray b. cardiology consult c. dopamine infusion d. epinephrine infusion e. prostaglandin infusion
  8. 8. ABCs + Dextrose MANTRA ABCs A: airway issues are a special consideration in kids with heart disease and other potential midline defects as part of a congenital syndrome (like choanal atresia (nasal passage doesn’t develop fully; this is a life-threatening event because infants only breathe through their nose) and Pierre Robin syndrome (their small jaws might make intubation difficult; 20% of kids with pierre robin will have a congenital heart defect, Pearl 1982) C: you want to get IV or IO access as soon as possible in a sick neonate. D: always check a sugar in a sick looking kid
  9. 9. ABCs + Dextrose MANTRA ABCs A: airway issues are a special consideration in kids with heart disease and other potential midline defects as part of a congenital syndrome (like choanal atresia (nasal passage doesn’t develop fully; this is a life-threatening event because infants only breathe through their nose) and Pierre Robin syndrome (their small jaws might make intubation difficult; 20% of kids with pierre robin will have a congenital heart defect, Pearl 1982) C: you want to get IV or IO access as soon as possible in a sick neonate. D: always check a sugar in a sick looking kid
  10. 10. 4 objectives 1. Become familiar with the common presentations of CHD in the neonate 2. Broadly classify the type of cardiac lesion (not the specific defect) 3. Establish a diagnostic game plan for yourself if you see this in your ER 4. Know how to treat a kid with CHD in extremis
  11. 11. Objective 1 LEARN THE COMMON PRESENTATIONS OF CONGENITAL HEART DISEASE
  12. 12. CYANOSIS SHOCK CHF BALANCED
  13. 13. 4 PRESENTATIONS IN PEDS CARDIAC PATIENTS Leftsided lesion Rightsided lesion Busy slide but has a lot of good info in it so I kept it intact Rapid onset of intense cyanosis strongly suggests a ductal dependent congenital heart defect. In left-sided lesions supplemental O2 should be used sparingly in these infants because high O2 levels will make the ductus close quicker
  14. 14. Objective 2 Classify the type of cardiac lesion. Not the specific defect (that’s what cardiologists are paid for)
  15. 15. Let’s review fetal circulation DA FO DV The umbilical vein brings oxygenated blood from placenta through DUCTUS VENOSUS to the IVC. Blood enters the RA where it goes through the FO to the LA, bypassing the RV and pulmonary circulation. Deoxygenated blood from upper body comes from the SVC to the RA and down to the RV and out the pulmonary artery. Since the pulmonary system is vasoconstricted only 10% goes to the lungs. The rest of the blood takes the path of least resistance into the DA, a connection to the descending aorta. When the baby takes its first breath the increase in O2 results in a huge decrease in pulmonary vascular resistance and blood starts flowing to the lungs. Overs hours to days the ductus and foramen ovale closes.
  16. 16. STRUCTURAL NONSTRUCTURAL Cardiac emergencies come in two flavors: structural and nonstructural non structural emergencies include arrhythmias (bradycardia and tachycardia) and disorders of myocardial function
  17. 17. STR UCT UR AL VOLUME OVERLOAD PRESSURE OVERLOAD (OBSTRUCTIVE)
  18. 18. VOLUME OVERLOAD VSD Total anomalous pulmonary venous return PDA ASD Truncus arteriosus Double outlet right ventricle AV canal Ebstein anomaly
  19. 19. VOLUME OVERLOAD 25% of CHD L R shunt can lead to right sided heart failure Can’t finish a feed Failure to thrive Hepatomegaly
  20. 20. Pressure Overload (Obstructive) AKA DUCTAL DEPENDENT LESIONS 1. CARDIOVASCULAR COLLAPSE 2. GRADUAL DYSFUNCTION will present in 2 ways The first, the more dramatic form presents in newborns with cardiovascular collapse because blood won’t be able to flow into the pulmonary or systemic circulation. The second is seen with INCOMPLETE forms of obstructive lesions that will gradually cause dysfunction
  21. 21. DUCTAL DEPENDENT LESIONS LEFT SIDED (BLOOD CAN’T GET TO BODY) RIGHT SIDED (BLOOD CAN’T GET TO LUNGS) each defect could be an hour lecture people do entire fellowships to learn this stuff trivia at this point for us same emergency treatment for all of them
  22. 22. DUCTAL DEPENDENT LESIONS IT LEFT SIDED (BLOOD CAN’T GET TO BODY) DOESN’T RIGHT SIDED (BLOOD CAN’T GET TO LUNGS) MATTER each defect could be an hour lecture people do entire fellowships to learn this stuff trivia at this point for us same emergency treatment for all of them
  23. 23. The Classic Cyanotic Congenital Heart Lesions Mnemonic time! If you’re dying to come away with this knowing a few congenital lesions these are probably the best ones to know for testing purposes. These are Right-sided lesions and will present as a cyanotic baby
  24. 24. TRUNCUS ARTERIOSUS 1 finger because aorta and pulm artery emerge as a single vessel allowing total mixing of deoxygenated and oxygenated blood. This is lesion will cause volume overload. Kids are born cyanotic.
  25. 25. TRANSPOSITION OF THE GREAT VESSELS aorta comes off the RV pulmonary artery comes off the LV you need some sort of mixing lesion to survive its both a mixing and obstructive lesion: mixing until the ductus closes then they develop severe cyanosis.
  26. 26. TRICUSPID ATRESIA tricuspid valve doesn’t form so blood won’t make it from the RA into the RV you need either a mixing lesion to get from from the right to left side then you need a PDA to get blood to the lungs
  27. 27. TETRALOGY OF FALLOT we’ll get to this one in a few slides but you put up four fingers because there are four features involved
  28. 28. TOTAL ANOMALOUS PULMONARY VENOUS RETURN 5 fingers because there are 5 words in the name pulmonary veins don’t return to the LA so no oxygenated blood pumped out of aorta unless you have a mixing lesion
  29. 29. Objective 3 How do you go about diagnosing this?
  30. 30. H&P VITALS HYPEROXIA TEST CXR/EKG DIFFERENTIAL DX We don’t see this all the time so we need a very concrete way of dealing with this The work up for CHD includes:
  31. 31. Trauma Seizures Heart Formula Endocrine Intestinal Metabolic Inborn errors The crashing neonate is scary having a go-to ddx might relieve some anxiety sepsis in a sick newborn until proven otherwise catastrophes Toxins Sepsis
  32. 32. HISTORICAL CLUES Poor feeding Irritability Diaphoresis with feeds (stress test) these suggest a heart issue
  33. 33. EXAM Murmur+ concerning history= get EKG and CXR Tachypnea CHF: hepatomegaly, gallop gallop= 3 or 4 heart sounds instead of 2
  34. 34. inverted T waves tall R waves Infant ECG with right ventricular hypertrophy. Signs of right ventricular hypertrophy include larger than normal amplitudes of R and inverted T waves in right precordial leads. Axis: normal newborns have a right axis deviation, normal QRS is RIGHT and ANTERIOR (+135 to +180) R waves will be higher in the right/septal precordial leads (V1 and V2) T waves are typically inverted in all the precordial leads Axis will slowly evolve into the normal leftward axis over the next few months If you see left axis deviation in the first week of life you should suspect a CHD
  35. 35. inverted T waves tall R waves Infant ECG with right ventricular hypertrophy. Signs of right ventricular hypertrophy include larger than normal amplitudes of R and inverted T waves in right precordial leads. Axis: normal newborns have a right axis deviation, normal QRS is RIGHT and ANTERIOR (+135 to +180) R waves will be higher in the right/septal precordial leads (V1 and V2) T waves are typically inverted in all the precordial leads Axis will slowly evolve into the normal leftward axis over the next few months If you see left axis deviation in the first week of life you should suspect a CHD
  36. 36. You won’t dx CHD on CXR but it might make you more suspicious In kids, cardiomegaly is usually defined as a cardiac silhouette >60% of the AP diameter Remember, the thymus can make reading infant xrays difficult. So get a lateral to look for true cardiomegaly. Boot shaped heart chest xray in an infant with tetralogy of fallot shape results from right ventricular hypertrophy due to right ventricular outflow tract obstruction Tetralogy of Fallot accounts for 10% of the cases of congenital heart disease. It is the most common cyanotic heart defect tet spell is a cyanotic episode due to worsening of the R to L shunt
  37. 37. Tetralogy of Fallot KNEE TO CHEST/ BOLUS 1. VSD SVR 2. RV outflow tract narrowing phenylephrine 3. Overriding aorta MORPHINE PVR 4. RV hypertrophy OXYGEN You won’t dx CHD on CXR but it might make you more suspicious In kids, cardiomegaly is usually defined as a cardiac silhouette >60% of the AP diameter Remember, the thymus can make reading infant xrays difficult. So get a lateral to look for true cardiomegaly. Boot shaped heart chest xray in an infant with tetralogy of fallot shape results from right ventricular hypertrophy due to right ventricular outflow tract obstruction Tetralogy of Fallot accounts for 10% of the cases of congenital heart disease. It is the most common cyanotic heart defect tet spell is a cyanotic episode due to worsening of the R to L shunt
  38. 38. Another classic xray finding in CHD is known as the Egg on a String Narrowing of superior mediastinum (anterior position of aorta) and globular shape of heart in neonates with transposition of great arteries
  39. 39. Snowman sign- total anomalous pulmonary venous return Again, it doesn’t matter what the specific defect is. As long as you can determine this xray doesn’t look right you’ve done your job
  40. 40. VITALS 4 extremity BPs Pre and post ductal O2 saturations two unique vital signs to check in a kid with suspected CHD preductal sat will be from the right wrist or finger post ductal from the lower extremities in coarctation of the aorta you’ll have low lower extremity BPs and lower post ductal sats
  41. 41. Hyperoxia Test Answers the question: Is it a lung problem or a heart problem? Textbook: 1. Get an ABG on room air 2. Put patient on 100% O2 for 10 mins 3. Get another ABG If it’s a lung problem the PaO2 will be >150 mmHg If it’s a cardiac problem it will be <100 Quick and dirty: Put kid on 100% O2 and see if their sats increase If the kid’s O2 sat doesn’t respond you’re looking at a CHD and then you’re aiming for an O2 sat between 70-80% You don’t need a cardiologist or any other help to do this.
  42. 42. Hyperoxia Test Answers the question: Is it a lung problem or a heart problem? Textbook: 1. Get an ABG on room air 2. Put patient on 100% O2 for 10 mins 3. Get another ABG If it’s a lung problem the PaO2 will be >150 mmHg If it’s a cardiac problem it will be <100 Quick and dirty: Put kid on 100% O2 and see if their sats increase If the kid’s O2 sat doesn’t respond you’re looking at a CHD and then you’re aiming for an O2 sat between 70-80% You don’t need a cardiologist or any other help to do this.
  43. 43. Hyperoxia Test Answers the question: Is it a lung problem or a heart problem? Textbook: 1. Get an ABG on room air 2. Put patient on 100% O2 for 10 mins 3. Get another ABG If it’s a lung problem the PaO2 will be >150 mmHg If it’s a cardiac problem it will be <100 Quick and dirty: Put kid on 100% O2 and see if their sats increase If the kid’s O2 sat doesn’t respond you’re looking at a CHD and then you’re aiming for an O2 sat between 70-80% You don’t need a cardiologist or any other help to do this.
  44. 44. Objective 4 Know what to do if this kid comes into your ER
  45. 45. TAKE YOUR OWN PULSE
  46. 46. CLASSIFICATION OF LESION TEMPO OF PRESENTATION SEVERITY OF CLINICAL CONDITION aggressiveness of your therapy will be determined by: the type of lesion (whether its left sided or right sided) how fast they decompensated and how bad they look
  47. 47. BALANCE PULMONARY AND SYSTEMIC BLOOD FLOW (Qp=Qs)
  48. 48. BE CAREFUL WITH OXYGEN IF O2 IS NOT HELPING SHUT IT OFF SUSPECTED CHD: AIM FOR O2 75-85% THAT’S A GAS OF 7.4/40/40 remember, oxygen is a potent pulmonary vasodilator, it might make a left sided lesion worse making shock worse also a PDA will close with more O2
  49. 49. FOR SUSPECTED CHD (failed hyperoxia test) 10 cc/kg NS BOLUS IS A GOOD PLACE TO START for any super sick looking neonate you will rarely hurt them with O2 and a 20cc/kg NS bolus. If your suspicion for a congenital heart defect is high then you might want to be a little more careful with your oxygen and fluid bolus. it’s easier to add fluids than take them away
  50. 50. PROSTAGLANDINS PROSTAGLANDINS (PGE1) this is all you really need to remember from this talk its a strong vasodilator that has a direct effect on smooth muscle of ductus arteriosus you should consider this when any infant presents with severe hypoxemia or shock in the first few weeks of life decision to start a prostaglandin drip should be made clinically and not on a definite diagnosis
  51. 51. 0.03 to 0.1 mcg/kg/min Doesn’t require central access If you have extra support you’ll call cardiology and they will echo the kid Prostaglandin drip continues until they go to the OR
  52. 52. APNEA 12% FEVER 10% Elective intubation might be considered before transporting a kid requiring a prostaglandin infusion it’s probably a good idea to have your airway equipment by the bedside if you’re about to start infusing Fever is less of an issue because most of these sick looking kids will get a full septic work up anyways.
  53. 53. PRESSORS PROBLEM LEFT SIDED LESIONS (blood shunted TOWARD pulmonary circulation) RIGHT SIDED LESIONS (blood shunted AWAY from pulmonary circulation) SOLUTION Increase systemic circulation Decrease afterload MILRINONE/DOBUTAMINE Decrease systemic circulation Increase SVR EPI/NE/HIGH DOSE DOPA Qp:Qs = 1:1 your main job is to stabilize these kids and send them to an icu but if you’re stuck by yourself in a small ER and have to manage these kids without help you might have to start some pressors
  54. 54. Sodium Bicarb: “Basically Useless Therapy” “Insufficient data to recommend routine use of bicarb in resuscitation of the newly born. In fact, the hyperosmolarity and CO2 generating properties may be detrimental to myocardial or cerebral function” Evidence For Evidence Against Usher 1967 Simmons 1974 Papile 1978 Wakabayashi 1994 Marangoni 1995 Sirieix 1997 van Alfen-van der Velden 2006 Lipshultz 2003 Awada 2007 (Aschner. Pediatrics. 2008) The use of bicarb in crashing cardiac kids is controversial. Everyone does it but there’s really no evidence to show that it works. It probably does more harm than good. But if you’re in a code situation and you’ve tried everything and the kid still looks terrible no one will fault you for throwing in some bicarb. The point is that if you can’t ventilate the kid well then bicarb prob won’t help
  55. 55. Sodium Bicarb: “Basically Useless Therapy” “Insufficient data to recommend routine use of bicarb in resuscitation of the newly born. In fact, the hyperosmolarity and CO2 generating properties may be detrimental to myocardial or cerebral function” Evidence For Evidence Against Usher 1967 Simmons 1974 Papile 1978 Wakabayashi 1994 Marangoni 1995 Sirieix 1997 van Alfen-van der Velden 2006 Lipshultz 2003 Awada 2007 (Aschner. Pediatrics. 2008) The use of bicarb in crashing cardiac kids is controversial. Everyone does it but there’s really no evidence to show that it works. It probably does more harm than good. But if you’re in a code situation and you’ve tried everything and the kid still looks terrible no one will fault you for throwing in some bicarb. The point is that if you can’t ventilate the kid well then bicarb prob won’t help
  56. 56. QUICK COMMENT ON KIDS BETWEEN STAGES OF CHD REPAIR Some kids are completely supported by a single surgical intracardiac shunt These shunts might clot Can’t open a PDA anymore Bolus with fluids, pressors, call cards, Needs to go to OR For the really bad lesions like hypoplastic left heart the repair process is made in stages as the kid grows. Partially corrected kids might present to you crashing.
  57. 57. THE 10% YOU SHOULD TAKE AWAY FROM THIS AVAILABILITY BIAS Get IV/IO access ASAP THE MISFITS HYPEROXIA TEST PROSTAGLANDINS 0.03-0.1 mcg/kg/min APNEA These conditions are rare but not THAT rare. Have a healthy respect for them and look for the needle in the haystack if a doesn’t look well Know how to put an I/O in a kid THE MISFITS mnemonic will give you the differential for a crashing baby: trauma, heart, endocrine, metabolic, inborn errors, seizures, formula issues, intestinal catastrophes, toxins, sepsis Put the kid on 100% oxygen and see if their sats go up at all. If not, aim for sats between 75-85% with as minimal O2 as possible Have a low threshold to start prostaglandins on super sick looking newborns that don’t respond to oxygen But be prepared to intubate them if they go apneic
  58. 58. THANK YOU GOOD LUCK AND TRY NOT TO SUCK OUT THERE

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