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  1. 1. CARDIOLOGY<br /><ul><li>General aspects
  2. 2. Blood pressure
  3. 3. Chest pain
  4. 4. Know that chest pain in healthy children is generally not cardiopulmonary in origin
  5. 5. Recognize the CV causes of chest pain
  6. 6. Pericarditis: substernal chest pain with a squeezing or tightening character, worse with movement and lying down; feels better if they lean forward
  7. 7. Arrhythmias: especially SVT; pain improves when the arrhythmia resolves
  8. 8. Aortic dissection: possible if kid with Marfan of Ehler-Danlos
  9. 9. Syncope
  10. 10. Understand that the description of a syncopal episode usually directs the evaluation
  11. 11. Neurocardiogenic syncope: most common form. Almost always benign.
  12. 12. Occurs most commonly while person is standing, especially for long periods of time, but can occur with emotional stress or noxious stimuli (like blood). Usually have a prodrome of dizziness, nausea, change in hearing and vision.
  13. 13. MUST get a good famhx to rule out potential familial syndromes (like long QT)
  14. 14. Syncope with exercise is almost always abnormal and needs further eval (see below)
  15. 15. Good place to start for dx work up is an EKG even if suspect neurocardiogenic
  16. 16. Cardiac causes of syncope would include heart block, prolonged QT, sinus node dysfxn and pre-excitation syndromes (WPW)
  17. 17. Know the importance of CV eval in pts with syncopal or pre-syncopal episodes with exercise
  18. 18. Needs a complete and thorough CV eval and pt must not exercise until eval completed and dx made
  19. 19. Can include hypertrophic cardiomyopathy, arrhythmias and anomalies of the coronary arteries
  20. 20. Family hx is especially important, but even if it is negative they still need a w/u by a cardiologist
  21. 21. Murmur
  22. 22. Recognize the qualities of innocent heart murmurs and provide appropriate counseling
  23. 23. Most innocent murmurs:
  24. 24. Early systolic ejection
  25. 25. Short duration
  26. 26. Low intensity (grade 1 or 2)
  27. 27. Vibratory or musical quality
  28. 28. Still murmur
  29. 29. SEM, musical/vibratory like a plucked string
  30. 30. Heard best at lower precordium and decreases with inspiration and standing (decreased venous return)
  31. 31. PPPS (physiologic peripheral pulmonic stenosis)
  32. 32. Soft systolic ejection murmur heard best in the axillae and both hemithoraces
  33. 33. Due to the acute take off angle of branch pulmonary arteries and usually resolves by age 12 months
  34. 34. Other innocent murmurs include basal ejection systolic murmur, supraclavicular arterial bruit, venous hum
  35. 35. Recognize that a child with an innocent murmur requires no further evaluation
  36. 36. CHF
  37. 37. Diagnosis
  38. 38. Recognize irritability, dyspnea during feeding, and decreased volume with each feeding as sx of CHF in infants
  39. 39. CHD is the most common reason for CHF in children, and it usually develops during infancy
  40. 40. Due to increased workload on the cardiac muscle usually caused by structural defects
  41. 41. Excessive volume load: large AV septal defect, large VSD
  42. 42. Excessive pressure load: aortic stenosis, coarctation
  43. 43. Excessive volume and pressure: large VSD with coarctation
  44. 44. Less commonly due to actual problems with the myocardial performance, which can arise fro an inflammatory or infectious process that directly affects the myocardium and affects its contractility
  45. 45. Recognize si and sx of CHF
  46. 46. See above and next
  47. 47. Identify the importance of physical findings (e.g. edema, hepatomegaly, JVD, cardiomegaly, gallop rhythm) in CHF in older kids
  48. 48. The PREP questions like to point out this gallop rhythm; it is due to diminished systolic and diastolic function of the LV
  49. 49. As LV dysfunction increases, the right heart becomes affected as the increased pressure from the LV is transmitted through the pulmonary vascular system and then to the right heart (increased pressure against which the RV must pump); R sided heart failure leads to these classis findings of the hepatomegaly, SOB, crackles (less commonly seen in kids that adults), JVD
  50. 50. In older kids a dilated cardiomyopathy is a dx to consider with presentation of new CHF; for boards purposes think of this when they mention the kid having a recent URI
  51. 51. Know how an imaging study of the chest may help dx CHF
  52. 52. Enlarged cardiac shadow due to LVH my be seen
  53. 53. Pulmonary vascular congestion, pulmonary edema, effusions
  54. 54. Understand the association between systemic AV malformation and CHF in a newborn
  55. 55. A systemic AV malformation is essentially an extracardiac LR shunt
  56. 56. Blood flows via the AVM to the venous return and thereby overwhelms the right heart and results in right sided HF with its associated si/sx
  57. 57. These AVMs are often in the liver or brain
  58. 58. A murmur heard over a fontanelle = AVM
  59. 59. Recognize common causes of CHF in infants and children
  60. 60. Understand the role of the pulmonary vascular bed in the presentation of CHF in infants with large LR shunts
  61. 61. As the pulmonary vascular bed resistance decreases during the initial days/weeks of life, and the pulmonary pressures drop below the systemic pressures, the L R shunting will increase and therefore the condition will worsen. The left heart faces a higher afterload, and therefore there is increased back pressure to the pulmonary vasculature, and when it has a lowered resistance, the increased pressure from the LV is transmitted against the pulm vasculature and then to the R heart
  62. 62. Signs of R heart failure become evident as this occurs
  63. 63. Management
  64. 64. Plan the tx of CHF
  65. 65. Diuresis, diuresis, diuresis
  66. 66. Even when it does not yield a significant improvement in sx, it can be useful in improving lung fxn preoperatively
  67. 67. Congenital Heart Disease
  68. 68. General
  69. 69. Recognize the increased risk and plan appropriate eval of CHD in a newborn with congenital anomalies (e.g. trisomy 21, 18, FAS, 22q11, 45XO)
  70. 70. Need to et an echo early on in order to look for any associated CHD
  71. 71. Cri du Chat = VSD
  72. 72. Turner = Bicuspid aortic valves, coarctation
  73. 73. Tri 21 = Endocardial cushion defect
  74. 74. Tri 18 = VSD
  75. 75. Tri 13 = VSD
  76. 76. Cardiogenic shock
  77. 77. Know that and EKG and echo should be part of the eval of a patient with possible cardiogenic shock
  78. 78. Cardiogenic shock can mimic sepsis, especially in infants
  79. 79. Since cardiogenic shock is so immediately critical and life threatening, need to rule it out as quickly as possible, therefore doing the EKG and echo early and fast is warranted
  80. 80. Other studies, like a CBC and blood cx, can wait per PREP, and LPs can make the condition worse
  81. 81. Know that cardiogenic shock may be the initial finding in a newborn infant with CHD
  82. 82. Recognize findings of cardiogenic shock in the newborn
  83. 83. Gallop rhythm, hepatomegaly, tachypnea, lethargy, dehydration later signs, which are c/w the actual shock, are tachycardia, hypotension, decreased pulses/perfusion at which point the shock has gone from compensated to uncompensated
  84. 84. Know the tx of cardiogenic shock in the newborn infant
  85. 85. Giving fluids will worsen cardiogenic shock because it causes worsening congestion in the pulmonary circuit and adds more volume load to the already failing/dilated LV
  86. 86. If fluids are given to a pt in cardiogenic shock, will likely see and increase in HR as the heart attempts to increase CO (but is unable to increase SV due to poor pump)
  87. 87. The treatment = inotropics (dopamine) to increase contractility and thereby increase SV and CO
  89. 89. Cyanotic Dz
  90. 90. Distinguish between central cyanosis and acrocyanosis
  91. 91. Acrocyanosis = transient bluish discoloration of the hands and feet in response to vasomotor instability or a cold environment. The perioral region can also be involved (spares the lips and mucous membranes), and the extremities may be cool on examination
  92. 92. Central cyanosis = due to deoxygenated blood or reduced hgb concentration (usually in the range of 4-6g/dL). Affected infants have bluish discoloration of the lips, tongue, mucous membranes, and occasionally nail beds. Cyanosis is usually clinically apparent when the O2 sat <70-80%
  93. 93. Causes = right to left shunt due to CHD or respiratory disease, hypoventilation, methemogobinemia
  94. 94. ID the clinical features of a tet spell
  95. 95. TOF =
  96. 96. RV outflow/pulmonary stenosis
  97. 97. VSD
  98. 98. Overriding aorta
  99. 99. RVH
  100. 100. Tet spell in an infant = distress, crying, inconsolability, hyperpnea, increased cyanosis, also during a tet spell, the murmur will be diminished or absent b/c the murmur is due to pulm stenosis (decreased volume or RH output therefore = decreased murmur)
  101. 101. Often occur in the morning or times of dehydration the spell is brought on by diminished pulmonary blood flow
  102. 102. Tx = increase pulm blood flow
  103. 103. Can be accomplished immediately by placing the patient in a knee to chest or a squatting position which will increase venous return and also increase systemic resistance
  104. 104. Increase in systemic resistance can also be accomplished pharmacologically
  105. 105. Know the cardiac causes of cyanosis in a newborn (cyanotic hours to days after birth)
  106. 106. TOF will present with cyanosis in the newborn period only when the pulmonary stenosis is severe and causes a significant RL shunt at the VSD
  107. 107. Transposition of Great Arteries (TAG) most common form of cyanotic heart disease to present in the first day after birth (overall is the second most common cyanotic heart disease, after TOF); the LV connects to the pulm artier and the RV connects to the aorta so that deoxygenated blood returning via the SVC into the RA enters the RV and then back out the aorta (not oxygenated). They can be profoundly cyanotic if there is no reliable method for mixing left and right sided blood (left sided/oxygenated blood into the right side via and ASD or VSD) These babies are often otherwise normal, healthy appearing babies
  108. 108. Tricuspid atresia (anatomy review: they do not have a tricuspid valve, therefore blood from the RA cannot get to the RV, and the only way it can get out of the RA would be through an ASD, taking blood from the RA to the LA to the LV; once in the LV the only way for blood to get oxygenated is via a left to right shunt across a VSD into the RV where it can then go to the lungs). The obligate right to left shunt of desaturated blood from the RA to the LA , then to the LV and then systemic causes the early cyanosis
  109. 109. Truncus Arteriosusoccurs when a single arterial outlet supports the coronary, systemic and pulmonary blood flow. Cyanosis occurs when the origins of the pulm arteries from the truncus are narrowed
  110. 110. Total Anomalous Pulm Venous Return usually lack a direct connection between the pulm veins and the LA; the pulm veins drain into the RA or into veins that eventually drain into the RA. There are three forms, depending on where the connection occurs. Supracardiac will drain into the left innominate vein and then into the SVC. Cardiac drain directly to the RA or coronary sinus. Infracardiac (subdiaphragmatic) go below the diaphragm, connect with the ductus venosus and then into the IVC. This third kind is most likely to have obstructed flow and therefore early cyanosis. Usually FTT and tachypnea are presenting signs, but if they have a severe obstruction, the cyanosis may be the presenting sign and pulm edema can develop rapidly
  111. 111. Recognize the absence of improvement in arterial oxygen content with 100% oxygen in comparison with room air is compatible with the dx of cyanotic CHD
  112. 112. Know the complications of polycythemia in a patient with CHD
  113. 113. Polycythemia leads to increased blood viscosity and can cause thrombotic events
  114. 114. If a pt has CHD that cannot be corrected, partial volume exchange transfusions may be necessary to maintain Hct <65% or lower depending on signs and symptoms of complications of polycythemia
  115. 115. Understand the prognosis for a patient with TOF
  116. 116. Surgical survival of >95%
  117. 117. Understand the prognosis for cognitive development in patients with cyanotic congenital heart dz
  118. 118. Most kids who’ve had cyanotic CHD, even after early repair, are likely to have some degree of cognitive impairment
  119. 119. Outcome is related to degree of pre-op hypoxia, intraoperative management (cardiac bypass time), and post op complications
  120. 120. If they have abnormal findings on neurologic exam they are more likely to have poorer school performance than kids with same lesions and no neurologic findings
  121. 121. If their lesions do not require surgical repair they are less likely to have poorer school performance
  122. 122. Kids with acyanotic heart disease are less likely to have poorer school performance than those with cyanotic heart disease
  123. 123. Know that relative anemia can be associated with a stroke in a patient with cyanotic CHD
  124. 124. Can be related to iron-deficient blood with decreased O2 carrying capacity as well as structural changes in the erythrocytes made under the iron-poor environment that can cause a higher viscosity despite the anemia
  125. 125. Know the immediate management of a child with a hypoxic episode
  126. 126. Best way to increase O2 delivery is through PRBC transfusion
  127. 127. Understand the role of ductus arteriosus in cyanotic CHD and the use of PGE-1 tx
  128. 128. Acyanotic heart disease
  129. 129. Recognize the major clinical findings in patients with cardiac anomalies such as VSD, ASD, PDA and aortic stenosis or pulmonic stenosis
  130. 130. ASD exercise intolerance due to left to right shunting, systolic murmur without a click (due to increased flow across the pulmonic valve, not due to flow through the ASD), fixed and split second heart sound due to increased time required for the dilated right ventricle to empty its contents
  131. 131. VSD usually a holosystolic murmur caused by the left to right shunt from LV to RV beginning with onset of systole. If small, the murmur may be high pitched and heard best along the sternal border. The second heart sound is normal.
  132. 132. This is the most common congenital heart defect
  133. 133. Majority close within one year
  134. 134. Symptoms would arise from increased strain on the RV due to increased volume/pressure as the systemic resistance increases and the LR shunt across the defect increases during the first few weeks of life, usually sx develop at about 4-8 weeks of age
  135. 135. PDAproduces a continuous machinery-like murmur that is usually loudest at the left infraclavicular area. If the opening is large there may be increased aortic pulse pressure and bounding pulses
  136. 136. Aortic stenosisis associated with a systolic ejection click and a murmur best heard at the RUSB with radiation to the neck. The findings do not change with position. An infant with severe congenital AS may present fairly early with the findings of the murmur, diminished perfusion and pulses, signs of pulmonary edema and also may appear to be in septic shock. If it does not present in newborn period it will present at some point in later infancy or childhood because the problem gets worse as the kid gets bigger and the stenosis becomes more critical and the LV wears out
  137. 137. Pulmonic stenosissystolic ejection murmur at the LUSB with an associated opening click, the murmur often radiates to the back and the axillae as the sound of turbulence flows through the branch pulmonary arteries. This is the second most common CHD after VSD. A critical stenosis can present shortly after birth because the RV cannot effectively pump against the stenotic valve. Cyanosis can be present due to right to left shunting at the level of the atria. They are ductal dependent in order for blood to get to the lungs, it has to traverse the PDA in order to enter the pulmonary artery; therefore they present as/when the duct is closing with severe cyanosis and cardiac collapse, but in general it is not a cyanotic lesion except in the critical newborn. The majority of affected children have no other associated sx but need to be monitored over time
  138. 138. Know the importance of PDA in the presentation of hypoplastic left heart syndrome and in coarctation of the aorta
  139. 139. In cases severe coarctation, keeping the PDA open can help relieve an acute aortic obstruction (since the coarctation is often due to a posterior shelf into the aorta that is created by the closure of the PDA due to a defect in the vessel media)
  140. 140. Note: clinically severe coarctation can mimic AS
  141. 141. Hypoplastic left heartan underdeveloped left heart is basically nonfunctional and so the RV must pump for both pulmonary and systemic blood delivery via the PDA. If the PDA is not kept open, then there is no way for blood to go systemic
  142. 142. Plan the initial management of a premature infant with PDA
  143. 143. Give IV indomethacin or ibuprofen-lysine in 3 successive doses.
  144. 144. If this does not close the PDA then may need surgical ligation.
  145. 145. Do not give the ibuprofen before you have echocardiographic confirmation of the PDA
  146. 146. Understand the immediate (e.g. referral) and long term (i.e. frequent BP measurements) management in a patient with coarctation
  147. 147. Because it can eventually cause left heart failure
  148. 148. Infectious and postinfectious diseases
  149. 149. Infective endocarditis
  150. 150. Know the indications for abx ppx in children with congenital heart lesions
  151. 151. Prosthetic cardiac valve or prosthetic material used for valve repair
  152. 152. Previous infective endocarditis
  153. 153. CHD:
  154. 154. Unrepaired cyanotic CHD, including palliative shunts and conduits
  155. 155. Completely repaired CHD with prosthetic material or device placed in the preceding 6 months
  156. 156. Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device
  157. 157. Cardiac transplant recipients who develop cardiac valvulopathy
  158. 158. Procedures that require ppx = any dental procedure that require extensive manipulation of the gingival or when perforation of the oral mucosa is likely; it is also reasonable to provide ppx for procedures involving the respiratory tract, infected skin, or musculoskeletal tissue; GI and GU tract procedures do not require ppx
  159. 159. Know the drugs of choice for the ppx of infective endocarditis
  160. 160. Oral amoxicillin (50mg/kg) can be given 30-60 mins prior to the procedure
  161. 161. If pcn allergic then clinda or cephalexin; if can’t do PO can do ampicillin, if can’t do PO and also pcn allergic then IV clinda
  162. 162. Know the clinical manifestations of infective endocarditis
  163. 163. Prolonged fever despite antibiotics, constitutional sx including anorexia, weight loss, malaise, night sweats, arthralgias, myalgias, splenomegaly, Janeway lesions, splinter hemorrhages, hematuria, glomerulonephritis, Roth spots in the eyes, Osler nodes
  164. 164. Cardiac manifestations include murmur, usually due to valvular insufficiency, possibly CHF
  165. 165. Know the management of infective endocarditis
  166. 166. Obtain blood cx from 3 to 5 sites prior to starting abx
  167. 167. 4-6 weeks of abx usually required
  168. 168. May need surgery if they develop CHF or severe regurg
  169. 169. Know the microbiology of infective endocarditis
  170. 170. Strep viridans (S. mitis and S. bovis) as well as staph aureus are the most common bacterial pathogens in kids
  171. 171. Enterococcus, coag neg staph, fungi and th HACEK organisms can also cause it
  172. 172. (HACEK = Haemophilus sp, Actinobacillus actinomycetemcomitants, cardiobacterium hominis, elkenella corrodens, kingella kingae) – these are gram negative oral and pharyngeal flora that are fastidious and slow growing and require special media to culture
  173. 173. Know the epidemiology of infective endocarditis, including risk factors
  174. 174. Know that a blood cx is the most important test for the dx of infective endocarditis
  175. 175. Get multiple cx before starting abx, do not need to wait until the pt is febrile as they are constantly bacteremic
  176. 176. Rheumatic fever
  177. 177. Identify the clinical manifestations of rheumatic fever
  178. 178. JONES CRITERIA
  179. 179. 5 major clinical manifestations
  180. 180. Carditis
  181. 181. Chorea
  182. 182. SubQ nodules
  183. 183. Polyarthritis
  184. 184. Erythema marginatum
  185. 185. Minor manifestations
  186. 186. Arthralgia
  187. 187. Increased ESR
  188. 188. Prolonged PR interval
  189. 189. Fever
  190. 190. Increased CRP
  191. 191. For dx must have 2 major or 1 major + 2 minor and evidence of recent or concurrent strep pyogenes infection (group A strep)
  192. 192. Know the lab findings of rheumatic fever
  193. 193. For dx there must be either a positive throat cx for GAS, or a positive rapid strep test, or elevated or rising ASO/strep antibody titer
  194. 194. Elevated ESR, CRP are minor diagnostic criteria
  195. 195. Identify the murmurs of mitral insufficiency and aortic insufficiency as the most common murmurs in rheumatic fever
  196. 196. Plan the initial management of acute rheumatic fever
  197. 197. Penicillin is always given in acute rheumatic fever (emycin if pcn allergic) then ppx begins immediately after acute tx
  198. 198. Salicylates and steroids for controlling acute sx (carditis and chorea)
  199. 199. The ppx management is continued for 5 years or until age 21; either a monthly pcn injection or BID pcn v-k
  200. 200. Myocarditis
  201. 201. Identify the major clinical manifestations of myocarditis
  202. 202. Suspected when there is a new murmur, sudden cardiac failure, arrhythmia or a combination of these
  203. 203. Signs may be subtle and may be just fever, fatigue and new murmur
  204. 204. Sx get worse as the myocardial function diminishes
  205. 205. PE findings of tachycardia, tachypnea, and a holosystolic murmur of mitral regurg, diminished pulse and perfusion, hepatomegaly
  206. 206. More common in infants and young children than older children, has a seasonal predilection (more in spring and summer)
  207. 207. Know the lab eval of myocarditis
  208. 208. Most common viral pathogen is coxsackie B, but many viral and bacterial pathogens have been implicated
  209. 209. Pericarditis
  210. 210. Know the etiologies and clinical manifestations of pericarditis
  211. 211. Etiologies = viral, bacterial, inflammatory, rheumatologic
  212. 212. Chest pain = substernal, positional (worse when laying down) and can be severe and worsen with deep inspiration, coughing, or movement of the upper torso. Pts usually prefer to sit up or lean forward
  213. 213. Pericardial effusion can develop and can lead to tamponade
  214. 214. Friction rub may be heard, but not always, and not hearing it does not rule out pericarditis or effusion
  215. 215. Know the lab eval of pericarditis
  216. 216. Viral titers, ASO titers may help determine the causative organism, also testing of the pericardial fluid if obtained
  217. 217. Echo is the most useful dx test
  218. 218. EKG might show tachycardia, elevated ST segments, decreased QRS voltages or electrical alternans
  219. 219. Know the microbiology of pericarditis
  220. 220. Bacterial causes include staph aureus (most common bacteria) as well as n. meningitides, h. flu, s. pneumo
  221. 221. Viral causes are often coxsackie A/B, echovirus, adenovirus
  222. 222. Rheum = collagen vascular disease, rheumatoid arthritis
  223. 223. Other = postpericardiotomy syndrome
  224. 224. Know the pathogenesis of pericarditis
  225. 225. Most often viral, less often bacterial (see above)
  226. 226. Know the tx of pericarditis, including the importance of surgical drainage
  227. 227. Pericardiocentesis is needed when there is evidence of large effusion or compromise of cardiac function (tamponade)
  228. 228. Anti-inflammatory agents are the key treatment, sometimes prednisone
  229. 229. If bacterial etiology may tx with abx
  230. 230. Kawasaki dz
  231. 231. Understand the proper use of echo in the eval and management of pts with KD
  232. 232. If pt meets dx criteria for KD then the echo is required in order to look for evidence of carditis
  233. 233. If it is an atypical case, then echo findings can help in confirming dx
  234. 234. Identify the cardiac complications of KD and the timing of onset; understand the prevention and treatment of the complications and the importance of follow up evaluation
  235. 235. About 50% of cases will show carditis by the end of the first week (acute phase)of sx, dilation (ectasia) may also appear at this phase
  236. 236. Coronary artery aneurysm usually appears at week 2-4 (subacute phase); its incidence is reduced greatly (from about 25% to 3% if pt is txed with IVIg during the acute phase)
  237. 237. Valvulitis and myocarditis can also occur
  238. 238. Rate and rhythm disorders, ischemia
  239. 239. Identify the clinical manifestations of common cardiac arrhythmias
  240. 240. Atrial arrhythmias = SVT, atrial ectopic tachycardia, atrial flutter, atrial fibrillation
  241. 241. Ventricular arrhythmias = ventricular tachycardia, ventricular fibrillation
  242. 242. Understand the clinical significance of a prolonged corrected QT
  243. 243. Can lead to ventricular dysrhythmias and sudden death
  244. 244. Using EKG patterns, identify PACs, PVCs, SVT and v tach
  245. 245. Understand the tx of SVT
  246. 246. SVT is the most common symptomatic dysrhythmia in kids.
  247. 247. Rapid, regular rate with narrow QRS (rate often nears 300BPM)
  248. 248. If relatively stable give IV adenosine
  249. 249. If unstable/crashing, they need immediate synchronized cardioversion
  250. 250. The boards don’t like you to try doing vagal maneuvers all that much
  251. 251. Systemic Disease affecting the heart
  252. 252. Know that hyperthyroidism should be considered in the eval of a pt with persistent sinus tachy
  253. 253. Likely will provide other clues about hyperthyroidism like weight loss, heat intolerance, etc, if this is a question they ask
  254. 254. Main thing, need to tell if it is sinus tachy or a dysrhythmia
  255. 255. Recognize that pts with Marfan syndrome may have associated cardiac dz that precludes participation in sports
  256. 256. Cardiac abnormalities can include dilation or aneurysm of arterial vessels, mitral valve dysplasia/prolapse/dysfxn, possible also to have same probs with tricuspid valve
  257. 257. Need to have their heart okayed before they can play or practice sports
  258. 258. Know the CV conditions associated with Turner syndrome
  259. 259. Bicuspid aortic valve and coarctation of the aorta
  260. 260. Recognize the si/sx of SVC syndrome
  261. 261. SVC obstruction can be due to
  262. 262. Extrinsic compression (i.e. tumor)
  263. 263. Intrinsic obstruction (i.e. clot, surgical anastomosis)
  264. 264. Abnormal hemodynamics due to elevated right atrial pressures
  265. 265. Have signs of superficial venous distention, venous congestion and facial and upper extremity swelling; as it progresses the jugular veins may become affected and there can be cerebral edema/seizures/death
  266. 266. Know the importance of CV evaluation when there is a fam hx of hypertrophic cardiomyopathy, MD, or Marfan
  267. 267. Hypertrophic cardiomyopathy is autosomal dominant inheritance, so if a parent has it all the kids need to be screened early and regularly as they have a 50% chance of inheriting it
  268. 268. MD – get cardiomyopathy
  269. 269. Marfan – see above
  270. 270. Identify the CV risk factors in kids and eval properly
  271. 271. Hyperlipidemia/chlesterolemia/triglyceridemia; these are familial and question often give clue about a parent with high cholesterol levels or an early ischemic event; need to screen the kids for same problem
  272. 272. If a parent has an early CV event then the kids should have an eval/screening