Cardiology
Deepak Palakshappa
Paritosh Prasad
Ana Maria Rosales
EKG Interpretation
Approach to the EKG
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Indication for EKG: W/u for chest pain, syncope, cyanotic episodes, drug ingestion, CHD eval, palpitations, pericarditis, Kawasaki dz, myocarditis, rheumatic heart fever, FHx sudden death and electrolyte abn. (Emerg Med Clin North Am 2006;24:195)
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Basic EKG: 12 lead w/ 6 precordial leads and 3 limb leads (BMJ 2002;324:1382)
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Paper speed usually 25 mm/sec so each small box 0.04 msec, 5 boxes 0.20 msec
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Standard voltage is at 10 mm/mV; 1 mm = 0.1 mV; can be modified at request
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Leads: R and L arm, R and L leg give rise to I, II, III, aVL, aVR, aVF.
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Dipolar: I, II, III; represent differential from one lead to another
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In I, positive deflection of wave is signal traveling toward RA to LA
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In II, positive deflection of wave is signal traveling toward RA to LL
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In III,– positive deflection of wave is signal traveling toward LA to LL
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Unipolar: + deflect = center out to limb; aVR (RA), aVL (LA), aVF (LL)
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Pericardial leads: Views cardiac activity in the horizontal plain.
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Initial EKG read: Always take a systematic approach; check speed and voltage
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Rhythm: Regular or irregular; then if sinus (every P followed by QRS, constant PR)
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Rate: # of large (5 mm) boxes btw R waves; 1 = 300 bpm, 2 = 150, 3 = 100; pattern is 300, 150, 100, 75, 60, 50; can also use 1500/# small boxes
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Axis: If R + in limb lead, vector goes toward that lead; nml axis based on age
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R waves + I and + aVF = 0°-90° (noted as normal axis; but can be abn for age)
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R waves + I and – aVF = 0° to -90° (Left axis deviation) actually -30–90
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R waves – I and + aVF = 90°-180° (Right axis deviation)
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R waves – I and – aVF = neg 90° to -80° (Extreme right/NW deviation)
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Neonates w/ transitioning from R sided dominance; initially w/ R axis as nml
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P wave axis; if sinus then + I, +aVF, if not consider ectopic atrial pacer (EAP)
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P waves: Should be same morphology in a given lead, otherwise multi pacemakers
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2.5 mm wide in II and/or biphasic in V1 = p mitrale; left atrial enlargement
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2.5 mm high in II = p pulmonale; right atrial enlargement
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Q wave: Can be nml (II, III, aVF, V5, V6), max amp at 3–5 yr (0.6–0.8 mV nml)
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QRS complex: R:S ratio initially >1 in V1 and V2, and <1 in V5 and V6, at about 3 yo R:S ratio becomes <1 in V1 and V2, and >1 in V5 and V6; some pts w/ juvenile pattern until 8–12 yr. (Heart 2005;91:1626)
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EKG assessment of LVH very poor in pediatrics; sens 19.4%, spec 85%
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T wave: Progressive changes through childhood, very different than adult pattern
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1st 2–3 DOL upright T wave in V1–V3 normal, then inverts in 1st wk of life
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T wave becomes upright during childhood, starting w/ V3, then V2, then V1
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50% nml 3–5 yos have inverted T in V2, only 5%–10% nml 8–12 yo w/ inverted T.
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T wave in V5 and V6 should be upright in all ages. (Heart 2005;91:1626)
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Intervals: Interpretation varies based on age group. (Heart 2005;91:1626)
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PR: ↑ w/ ↑ vagal tone, heart block, endocarditis w/ abscess, hyperK, digoxin tox, short w/ pre-excitation (WPW), EAP, glycogen storage dz
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QRS: >0.08 msec if <8 yo or >0.10 msec if >8 yo = bundle branch block, junctional or ventricular rhythm (not via His Purkinje) (Emerg Med Clin North Am 2006;24:195)
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QT: Start of Q to end of T; correct for HR w/ Bazett formula QT/[check mark]RR
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Both old and recent reviews place upper limit nml QTc at 450 msec
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Age Dependent Changes
(Emerg Med Clin North Am 2006;24:195)
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Nml limits prev from Davignon et al. (2141 Caucasian pts), more recent by Rijnbeek et al. w/ higher sampling rate w/ sign. diff in nml limits (Euro Heart J 2001;22:702)
HR | PR Interval | QRS Axis | QRS Interval | QTc Limit | |
---|---|---|---|---|---|
0–1 wk | 90–160 | 0.08–0.15 | 60°–180° | 0.03–0.08 | <0.49 |
1wk–2 mo | 100–180 | 0.08–0.15 | 45°–160° | 0.03–0.08 | <0.49 |
2–6 mo | 105–185 | 0.08–0.15 | 0°–135° | 0.03–0.08 | <0.49 |
6 mo–1 yr | 110–170 | 0.07–0.16 | 0°–135° | 0.03–0.08 | <0.45 |
1–8 yr | 90–165 (1–2 yr)65–140 (>2 yr) | 0.09–0.17 | 0°–110° | 0.04–0.08 | <0.45 |
8–16 yr | 60–130 | 0.09–0.17 | -15°–110° | 0.04–0.09 | <0.45 |
>16 yr | 50–120 | 0.12–0.20 | -15°–110° | 0.05–0.10 | <0.45 |
Heart Murmurs
Definition
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Result of turbulent blood flow; can be 2/2 ↑ blood flow (fever, anemia), abn cardiac structures (abn valve, cardiac defect) or combination
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50%–70% seen annual exam, sports physicals, etc. w/ murmur on exam but only 0.8%–1% of pop w/ structural congenital heart disease. (Pediatr Rev 2007;28:e19)
Cardiac Examination
(Pediatr Rev 2007;28:e19)
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Observation for syndromic appearance, central cyanosis, breathing, JVP
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Palpation for thrills and point of max impulse for displacement, hyperdynamic flow
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Pulse exam: Bounding (inc pulse pressure; PDA, AR, hyperthyroid, AVF), pulsus parvus (weak)/tardus (late) in AS, unequal in all 4 ext (aortic coarc)
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Abdominal exam: Hepatosplenomegaly (CHF), pulsatile liver (TR)
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Auscultation characterizing S1 (AV valves) and S2 (aortic and pulmonic often split)
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S3 (rapid filling of ventric) often normal in children; sounds like slosh-ing-in
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S4 (snap of stiff ventricle) always pathologic; sounds like a-thick-wall
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Heart sound order; S4 — S1 —–S2—–S3; S2 nml split to A2–P2; can mistake for S3——slosh-ing—ina——thick- wall—–
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Murmurs: Define timing (systolic vs. diastolic; early, mid, late), intensity, location, quality, configuration (crescendo, decrescendo, etc.), duration.
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Systolic: Holosystolic (involves S1, cont to S2 at same intensity) and heard w/ AV valve regurg or VSDs; ejection murmurs (begin after S1 w/ cres-decresc) and related to flow in great vessels. (Pediatr Clin North Am 2004;51:1515)
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Diastolic: Almost always pathologic (aside from venous hum);
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Continuous: Flow through vessel/communication distal to aortic/pulm valves
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Pathologic (PDA; continuous machinery murmur) or benign (venous hum)
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Innocent Murmurs of Childhood
(Circulation 2005;111:e20; Pediatr Clin North Am 2004;51:1515)
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Stills murmur: Most common innocent murmur in children; 1st described in 1909
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Typically heard in patients aged 2–6 yo, but can be heard in infants and adolescents
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Vibratory systolic murmur, low pitched, best at LLSB radiating to apex
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2/2 turbulence in LV outflow tract; change w/ position and dec w/ Valsalva
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Pulmonary flow murmur: Cres-decres, early to mid-peaking systolic at LUSB
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Rough and dissonant, best heard in supine position; inc w/ expiration, dec upright
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Can be difficult to distinguish from ASD murmur but w/ ASD have fixed split S2
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Pulm stenosis distinguished by possible presence of thrill, ejection click, soft S2
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Peripheral pulmonary artery stenosis: Common <1 yr age, usually gone by 6 mo
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Low-/moderate-pitched ejection murmur in early/mid systole best at axilla or back
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In utero pulm outflow tract well developed, pulm arterial branches comparatively underdeveloped and arise at sharp angles, which resolves w/ growth
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May be difficult to distinguish btw this and pathologic periph pulm artery stenosis w/ Williams or rubella syndrome; murmur may persist beyond S2 w/ these.
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Supraclavicular flow murmurs: Cres-descres harsh, high-pitched 2/2 nml bld flow in aorta and head/neck vessels; hear best above the clavicles (e.g., over carotids)
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Same sitting or supine; diminished w/ shoulder girdle hyperextension (arms back)
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Aortic systolic flow murmur: Systolic ejection in aortic area 2/2 increased cardiac output; anxiety, anemia, hyperthyroidism, fever, extreme fitness.
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If murmur inc w/ dec preload (Valsalva, squat to stand) → HOCM
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Venous Hum: Most common type of continuous murmur and benign
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Best at infraclavicular region while sitting or standing; usually > on R side
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Diminished w/ supine position or pressure over jugular vein
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Pathologic Murmurs
(Circulation 2005;111:e20)
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Systolic – usually longer and louder than innocent counterparts
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Pansystolic: Involves/obscures S1; if constant; VSD, MR, TR; if crescendo, then PDA.
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Ejection (AS, PS): Signs of pathology are presence of ejection click, abn S2 split
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Assess pulses, presence of cardiac failure (JVD, etc.), diastolic murmur as well
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Diastolic: W/ exception of venous hum, all diastolic murmurs are pathologic
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Often need to reposition patient to best auscultate (sitting up leaning forward for aortic sounds and left lateral decubitus to best hear mitral sounds)
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Early: Usually decres; assoc w/ aortic or pulmonic regurgitation
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Mid: Cres-descres 2/2 inc flow across nml MV/TV or 2/2 MS/TS
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Late: Cres and also assoc w/ mitral or tricuspid stenosis (MS/TS)
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Continuous: Harsh machinelike murmur classic for PDA
Further Evaluation
(Circulation 2005;111:e20)
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Depends on clinical assessment of patient; if asymptomatic, exam is usually sufficient
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Echo is gold standard to assess cardiac structure; ancillary testing w/ EKG or CXR may be helpful; some suggest referral to pediatric cardiology before imaging.
Syncope
Definition
(Pediatr Rev 2000;21:384)
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Sudden, often brief loss consciousness and postural tone 2/2 ↓ cerebral blood flow
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Presyncope is the feeling one is about to pass out
Etiology
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Breath-holding spells: Incidence of 4.6% and primarily occur between 1 and 5 yr
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Always provoked by pain, anger, or frustration; normal physical and neuro exam
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Cyanotic type (80%): Peaks at 2 yo and resolves by 5 yo
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Characterized by a prodromal period of crying then forced expiration and apnea
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Involuntary Valsalva → ↑ intrathoracic pressure → ↓ cardiac output → ↓ cerebral blood flow, LOC, and loss of muscle tone
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May be assoc w/ generalized clonic jerks, opisthotonos, and brady
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Pallid type (20%): Preceded by frustration, pain, sudden startle, or minor trauma
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Initial quieting and breath holding → pallor → LOC and loss of muscle tone
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Abnormal slowing of HR w/ ocular compression seen in >50%
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Ocular compression test w/ at least 3 sec of asystole, followed by pallid syncope, and no epileptiform discharges on EEG confirms dx
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Neurocardiogenic (vasovagal): Because of autonomic dysfunction; strong FHx
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Usually seen in adolescents after prolonged standing in a crowded, warm environment
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Characteristically preceded by nausea, diaphoresis, light-headedness, or yawning
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Cardiac syncope
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Arrhythmogenic: Prolonged QT, WPW, heart block, sick sinus syndrome, SVT
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Structural: HOCM, severe aortic/pulmonic stenosis, pHTN, anom L coronary
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POTS (postural orthostatic tachycardia syndrome)
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Myxomas
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Neuropsychiatric
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Seizures/drop attacks
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Hyperventilation syndrome/panic attacks
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Hypoglycemia: gradual onset w/ weakness, hunger, sweating, agitation, confusion
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Migraines assoc w/ vertebrobasilar vascular spasm: HA persists after awakening
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Benign paroxysmal vertigo: sudden falling attacks w/ dizziness in pts <6 yo
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Cough syncope: Most common in children w/ asthma
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Recovery w/i seconds, and consciousness restored w/i minutes
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Clinical Manifestations
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Hx most important in selecting dx studies and guiding Rx
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Should include the time of day, time of last meal, and details of preceding activities
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Medication Hx including prescribed, OTC, and illicit drugs
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FHx: Sudden unexplained death, deafness, arrhythmias, congenital heart disease, sz, metabolic diseases, or MI at young age
Physical Exam
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Cardiac exam: Pulse, BP, orthostatics, murmurs, clicks; detailed neuro exam
Diagnostic Studies:
Guided by History and Physical Exam
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Measurement of serum glucose and electrolytes rarely of value unless an acute episode
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EKG: Assess rhythm, conduction, premature beats, delta waves, chamber enlargement, PR, QRS, and QTc; further testing w/ exercise tests or 24-hr Holter if needed
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Toxicology screen
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Echocardiography w/ Doppler studies
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Tilt table testing for positional syncope
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EEG: In pt w/ prolonged LOC, suspected sz; postictal, drowsiness or confusion
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Cardiology c/s indicated for pathologic heart murmur, CP preceding syncope, arrhythmia, ↑QTc, Q waves, RV strain (suggestive of pHTN), or LVH on EKG, or w/ FHx of cardiomyopathy or sudden death
Treatment
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Breath-holding spells: Reassurance and explanation of pathophysiology most important
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Iron therapy has been shown to decrease incidence in cyanotic type
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Consider anticholinergics in pallid type if they become severe or frequent
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Neurocardiogenic: Consider PO salt suppl +/- fludrocortisone over a few weeks
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Cardiac: Include drug therapy, radiofrequency ablation, or pacemaker placement
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Pts w/ long QT should not receive macrolides or cisapride
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Seizures: Appropriate anticonvulsants
Chest Pain
Definition
(Pediatr Clin North Am 2004;51:1553)
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Chest pain (CP) in the pediatric population is overwhelmingly benign, but can have significant impact on patients; ½ miss school, 69% self-limit activity.
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Source can be 2/2 musculoskeletal, respiratory, cardiac, GI, or nervous system.
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Incidence of chest pain 2/2 cardiac etiology <5%.
Epidemiology
(Pediatr Rev 1986;8:56)
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Primary complaint in 0.3%–0.6% of pediatric patients in ED or outpt care
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May be chronic lasting up to 6 mo in 15%–36% of patients, 1 yr in 8%
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Mean age of presentation is 12–14 yr.
Clinical Manifestations
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Detailed Hx: Describe\pain (location and duration) quality, radiation, severity, temporal assoc (w/ breathing, eating, activity), exacerb or alleviating factors
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In younger patients, assess for occult history of ingestion as well.
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Chest pain assoc w/ exertion, syncope, light-headedness, or palpitations is concerning.
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Family Hx of sudden death, HOCM, MVP, or personal Hx of Kawasaki concerning
Etiologies
(Pediatr Rev 1986;8:56; Pediatr Clin North Am 2004;51:1553)
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Cardiac: Rare; responsible for <5% of pediatric chest pain
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Mitral valve prolapse: 18% pts w/ MVP have chest pain, though pain not 2/2 valve prolapse, unclear if neuroendocrine or autonomic dysfunction
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Check flat, sitting, and standing for midsystolic click and late systolic murmur
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Association with anxiety exists; echo is gold standard to diagnose
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Pericarditis: Sharp and stabbing, often pleuritic and positional; improved w/ leaning forward; may have recent URI sx’s, fever. Viral cause most common
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Can be infectious, inflammatory (w/ CTDs), neoplastic, or 2/2 XRT
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Exam w/ pericardial rub; EKG w/ PR depressions and diffuse ST elevations across all leads. PR elevation in aVR most specific finding.
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Myocarditis can also p/w chest pain but usually 2/2 assoc pericarditis
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Coronary vasospasm: P/w crushing, diffuse chest pain w/ assoc SOB, diaphoresis, radiation to L arm, neck, or jaw; light-headedness/syncope.
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Exam may have gallop (S3 and S4), +/- signs of poor cardiac function
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Consider cocaine induced, check tox screen, and if suspected use combined α- and β-antagonist (pure β-antagonist → unopposed α activity and periph vasospasm)
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Can also see vaso-occlusive dz w/ some systemic dz’s; ex sickle cell
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Anomalous coronary artery: Rare; coronary arteries arise from opposite sinus of Valsalva increases risk for ischemia and sudden death
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Usually p/w sudden death but 5/27 in 1 study w/ CP in prior 2 yr
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Chest pain associated w/ exertion; often nml physical exam; usually silent or S3 and/or S4 (cardiac dysfunction)
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EKG and stress test have not shown to be helpful in identifying at-risk pts
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Kawasaki disease: If c/b coronary artery aneurysm, can see stenosis or aneurismal thrombus; if Hx prior Kawasaki w/ aneurysm and p/w CP, ischemia until proven not.
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LV outflow obstruction: Hypertrophic obstructive cardiomyopathy (HOCM) most common though rarely p/w chest pain; exam w/ systolic murmur at aortic region that amplifies w/ standing or Valsalva
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Pulm HTN: Unclear mech; may be 2/2 pulm art stretch or RV ischemia. (Am Fam Physician 2001;63:1789)
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Tachyarrhythmias: Abrupt onset and cessation, w/ or w/o activity, often w/ N/V.
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Exam usually normal; EKG may demonstrate delta wave if pre-excitation (Wolf-Parkinson-White w/ bypass tract).
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Idiopathic: 21% cases no cause identified in prospective study (Pediatrics 1988;82:319)
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Avg pt w/ wks to mos intermittent CP, sharp, w/ or w/o exertion, short duration, no assoc sx, recurrence common, PE nml, and pain not reproducible
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Musculoskeletal: 15% cases in prospective study (Pediatrics 1988;82:319)
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Strain or costochondritis from overuse or trauma. Reproducible on exam.
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Hx of exertion/activity, pain usually sharp and radiating, can be pleuritic
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Costochondritis w/ tenderness on palpation of site of rib attachment to sternum
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Precordial catch syndrome – sharp, well localized twinge of pain, acute onset at rest and lasts sec to min; not reproducible on palpation
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Slipping rib syndrome: 8th,9th,10th ribs slip over one another (Pediatrics 1985;76:810)
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