Cardiology



Cardiology


Deepak Palakshappa

Paritosh Prasad

Ana Maria Rosales



EKG Interpretation


Approach to the EKG



  • 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)


  • Basic EKG: 12 lead w/ 6 precordial leads and 3 limb leads (BMJ 2002;324:1382)



    • Paper speed usually 25 mm/sec so each small box 0.04 msec, 5 boxes 0.20 msec


    • Standard voltage is at 10 mm/mV; 1 mm = 0.1 mV; can be modified at request


    • Leads: R and L arm, R and L leg give rise to I, II, III, aVL, aVR, aVF.


    • Dipolar: I, II, III; represent differential from one lead to another



      • In I, positive deflection of wave is signal traveling toward RA to LA


      • In II, positive deflection of wave is signal traveling toward RA to LL


      • In III,– positive deflection of wave is signal traveling toward LA to LL


      • Unipolar: + deflect = center out to limb; aVR (RA), aVL (LA), aVF (LL)


      • Pericardial leads: Views cardiac activity in the horizontal plain.




image



  • Initial EKG read: Always take a systematic approach; check speed and voltage



    • Rhythm: Regular or irregular; then if sinus (every P followed by QRS, constant PR)


    • 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


    • Axis: If R + in limb lead, vector goes toward that lead; nml axis based on age



      • R waves + I and + aVF = 0°-90° (noted as normal axis; but can be abn for age)


      • R waves + I and – aVF = 0° to -90° (Left axis deviation) actually -30–90


      • R waves – I and + aVF = 90°-180° (Right axis deviation)


      • R waves – I and – aVF = neg 90° to -80° (Extreme right/NW deviation)


      • Neonates w/ transitioning from R sided dominance; initially w/ R axis as nml


      • P wave axis; if sinus then + I, +aVF, if not consider ectopic atrial pacer (EAP)


    • P waves: Should be same morphology in a given lead, otherwise multi pacemakers



      • 2.5 mm wide in II and/or biphasic in V1 = p mitrale; left atrial enlargement


      • 2.5 mm high in II = p pulmonale; right atrial enlargement


    • Q wave: Can be nml (II, III, aVF, V5, V6), max amp at 3–5 yr (0.6–0.8 mV nml)


    • 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)



      • EKG assessment of LVH very poor in pediatrics; sens 19.4%, spec 85%


    • T wave: Progressive changes through childhood, very different than adult pattern



      • 1st 2–3 DOL upright T wave in V1–V3 normal, then inverts in 1st wk of life


      • T wave becomes upright during childhood, starting w/ V3, then V2, then V1


      • 50% nml 3–5 yos have inverted T in V2, only 5%–10% nml 8–12 yo w/ inverted T.


      • T wave in V5 and V6 should be upright in all ages. (Heart 2005;91:1626)


    • Intervals: Interpretation varies based on age group. (Heart 2005;91:1626)



      • PR: ↑ w/ ↑ vagal tone, heart block, endocarditis w/ abscess, hyperK, digoxin tox, short w/ pre-excitation (WPW), EAP, glycogen storage dz


      • 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)


      • QT: Start of Q to end of T; correct for HR w/ Bazett formula QT/[check mark]RR


      • Both old and recent reviews place upper limit nml QTc at 450 msec



Age Dependent Changes

(Emerg Med Clin North Am 2006;24:195)



  • 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



  • Result of turbulent blood flow; can be 2/2 ↑ blood flow (fever, anemia), abn cardiac structures (abn valve, cardiac defect) or combination


  • 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)



  • Observation for syndromic appearance, central cyanosis, breathing, JVP


  • Palpation for thrills and point of max impulse for displacement, hyperdynamic flow



    • Pulse exam: Bounding (inc pulse pressure; PDA, AR, hyperthyroid, AVF), pulsus parvus (weak)/tardus (late) in AS, unequal in all 4 ext (aortic coarc)


    • Abdominal exam: Hepatosplenomegaly (CHF), pulsatile liver (TR)


  • Auscultation characterizing S1 (AV valves) and S2 (aortic and pulmonic often split)



    • S3 (rapid filling of ventric) often normal in children; sounds like slosh-ing-in


    • S4 (snap of stiff ventricle) always pathologic; sounds like a-thick-wall


    • Heart sound order; S4 — S1 —–S2—–S3; S2 nml split to A2–P2; can mistake for S3

      ——slosh-ing—in

      a——thick- wall—–


    • Murmurs: Define timing (systolic vs. diastolic; early, mid, late), intensity, location, quality, configuration (crescendo, decrescendo, etc.), duration.



      • 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)


      • Diastolic: Almost always pathologic (aside from venous hum);


      • Continuous: Flow through vessel/communication distal to aortic/pulm valves



        • Pathologic (PDA; continuous machinery murmur) or benign (venous hum)


Innocent Murmurs of Childhood

(Circulation 2005;111:e20; Pediatr Clin North Am 2004;51:1515)



  • Stills murmur: Most common innocent murmur in children; 1st described in 1909



    • Typically heard in patients aged 2–6 yo, but can be heard in infants and adolescents


    • Vibratory systolic murmur, low pitched, best at LLSB radiating to apex


    • 2/2 turbulence in LV outflow tract; change w/ position and dec w/ Valsalva


  • Pulmonary flow murmur: Cres-decres, early to mid-peaking systolic at LUSB



    • Rough and dissonant, best heard in supine position; inc w/ expiration, dec upright


    • Can be difficult to distinguish from ASD murmur but w/ ASD have fixed split S2


    • Pulm stenosis distinguished by possible presence of thrill, ejection click, soft S2


  • Peripheral pulmonary artery stenosis: Common <1 yr age, usually gone by 6 mo



    • Low-/moderate-pitched ejection murmur in early/mid systole best at axilla or back


    • In utero pulm outflow tract well developed, pulm arterial branches comparatively underdeveloped and arise at sharp angles, which resolves w/ growth


    • 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.


  • 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)



    • Same sitting or supine; diminished w/ shoulder girdle hyperextension (arms back)



  • Aortic systolic flow murmur: Systolic ejection in aortic area 2/2 increased cardiac output; anxiety, anemia, hyperthyroidism, fever, extreme fitness.



    • If murmur inc w/ dec preload (Valsalva, squat to stand) → HOCM


  • Venous Hum: Most common type of continuous murmur and benign



    • Best at infraclavicular region while sitting or standing; usually > on R side


    • Diminished w/ supine position or pressure over jugular vein


Pathologic Murmurs

(Circulation 2005;111:e20)



  • Systolic – usually longer and louder than innocent counterparts



    • Pansystolic: Involves/obscures S1; if constant; VSD, MR, TR; if crescendo, then PDA.


    • Ejection (AS, PS): Signs of pathology are presence of ejection click, abn S2 split



      • Assess pulses, presence of cardiac failure (JVD, etc.), diastolic murmur as well


  • Diastolic: W/ exception of venous hum, all diastolic murmurs are pathologic



    • Often need to reposition patient to best auscultate (sitting up leaning forward for aortic sounds and left lateral decubitus to best hear mitral sounds)


    • Early: Usually decres; assoc w/ aortic or pulmonic regurgitation


    • Mid: Cres-descres 2/2 inc flow across nml MV/TV or 2/2 MS/TS


    • Late: Cres and also assoc w/ mitral or tricuspid stenosis (MS/TS)


  • Continuous: Harsh machinelike murmur classic for PDA


Further Evaluation

(Circulation 2005;111:e20)



  • Depends on clinical assessment of patient; if asymptomatic, exam is usually sufficient


  • 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)



  • Sudden, often brief loss consciousness and postural tone 2/2 ↓ cerebral blood flow


  • Presyncope is the feeling one is about to pass out


Etiology



  • Breath-holding spells: Incidence of 4.6% and primarily occur between 1 and 5 yr



    • Always provoked by pain, anger, or frustration; normal physical and neuro exam


    • Cyanotic type (80%): Peaks at 2 yo and resolves by 5 yo



      • Characterized by a prodromal period of crying then forced expiration and apnea


      • Involuntary Valsalva → ↑ intrathoracic pressure → ↓ cardiac output → ↓ cerebral blood flow, LOC, and loss of muscle tone


      • May be assoc w/ generalized clonic jerks, opisthotonos, and brady


    • Pallid type (20%): Preceded by frustration, pain, sudden startle, or minor trauma



      • Initial quieting and breath holding → pallor → LOC and loss of muscle tone


      • Abnormal slowing of HR w/ ocular compression seen in >50%


      • Ocular compression test w/ at least 3 sec of asystole, followed by pallid syncope, and no epileptiform discharges on EEG confirms dx


  • Neurocardiogenic (vasovagal): Because of autonomic dysfunction; strong FHx



    • Usually seen in adolescents after prolonged standing in a crowded, warm environment


    • Characteristically preceded by nausea, diaphoresis, light-headedness, or yawning


  • Cardiac syncope



    • Arrhythmogenic: Prolonged QT, WPW, heart block, sick sinus syndrome, SVT


    • Structural: HOCM, severe aortic/pulmonic stenosis, pHTN, anom L coronary


    • POTS (postural orthostatic tachycardia syndrome)


    • Myxomas


  • Neuropsychiatric



    • Seizures/drop attacks


    • Hyperventilation syndrome/panic attacks


    • Hypoglycemia: gradual onset w/ weakness, hunger, sweating, agitation, confusion


    • Migraines assoc w/ vertebrobasilar vascular spasm: HA persists after awakening


    • Benign paroxysmal vertigo: sudden falling attacks w/ dizziness in pts <6 yo


  • Cough syncope: Most common in children w/ asthma



    • Recovery w/i seconds, and consciousness restored w/i minutes


Clinical Manifestations



  • Hx most important in selecting dx studies and guiding Rx


  • Should include the time of day, time of last meal, and details of preceding activities



    • Syncope at rest/recumbent suggests sz or arrhythmias


    • Syncope w/ exercise suggests HOCM



    • Syncope while standing suggests vasovagal


    • Syncope w/o warning suggests primary cardiac


  • Medication Hx including prescribed, OTC, and illicit drugs


  • FHx: Sudden unexplained death, deafness, arrhythmias, congenital heart disease, sz, metabolic diseases, or MI at young age


Physical Exam



  • Cardiac exam: Pulse, BP, orthostatics, murmurs, clicks; detailed neuro exam


Diagnostic Studies:

Guided by History and Physical Exam



  • Measurement of serum glucose and electrolytes rarely of value unless an acute episode


  • 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


  • Toxicology screen


  • Echocardiography w/ Doppler studies


  • Tilt table testing for positional syncope


  • EEG: In pt w/ prolonged LOC, suspected sz; postictal, drowsiness or confusion


  • 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



  • Breath-holding spells: Reassurance and explanation of pathophysiology most important



    • Iron therapy has been shown to decrease incidence in cyanotic type


    • Consider anticholinergics in pallid type if they become severe or frequent


  • Neurocardiogenic: Consider PO salt suppl +/- fludrocortisone over a few weeks


  • Cardiac: Include drug therapy, radiofrequency ablation, or pacemaker placement



    • Pts w/ long QT should not receive macrolides or cisapride


  • Seizures: Appropriate anticonvulsants


Chest Pain


Definition

(Pediatr Clin North Am 2004;51:1553)



  • Chest pain (CP) in the pediatric population is overwhelmingly benign, but can have significant impact on patients; ½ miss school, 69% self-limit activity.


  • Source can be 2/2 musculoskeletal, respiratory, cardiac, GI, or nervous system.


  • Incidence of chest pain 2/2 cardiac etiology <5%.


Epidemiology

(Pediatr Rev 1986;8:56)



  • Primary complaint in 0.3%–0.6% of pediatric patients in ED or outpt care


  • May be chronic lasting up to 6 mo in 15%–36% of patients, 1 yr in 8%


  • Mean age of presentation is 12–14 yr.


Clinical Manifestations



  • Detailed Hx: Describe\pain (location and duration) quality, radiation, severity, temporal assoc (w/ breathing, eating, activity), exacerb or alleviating factors


  • In younger patients, assess for occult history of ingestion as well.


  • Chest pain assoc w/ exertion, syncope, light-headedness, or palpitations is concerning.


  • 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)



  • Cardiac: Rare; responsible for <5% of pediatric chest pain



    • Mitral valve prolapse: 18% pts w/ MVP have chest pain, though pain not 2/2 valve prolapse, unclear if neuroendocrine or autonomic dysfunction



      • Check flat, sitting, and standing for midsystolic click and late systolic murmur


      • Association with anxiety exists; echo is gold standard to diagnose


    • Pericarditis: Sharp and stabbing, often pleuritic and positional; improved w/ leaning forward; may have recent URI sx’s, fever. Viral cause most common



      • Can be infectious, inflammatory (w/ CTDs), neoplastic, or 2/2 XRT


      • Exam w/ pericardial rub; EKG w/ PR depressions and diffuse ST elevations across all leads. PR elevation in aVR most specific finding.


      • Myocarditis can also p/w chest pain but usually 2/2 assoc pericarditis


    • Coronary vasospasm: P/w crushing, diffuse chest pain w/ assoc SOB, diaphoresis, radiation to L arm, neck, or jaw; light-headedness/syncope.



      • Exam may have gallop (S3 and S4), +/- signs of poor cardiac function


      • Consider cocaine induced, check tox screen, and if suspected use combined α- and β-antagonist (pure β-antagonist → unopposed α activity and periph vasospasm)


      • Can also see vaso-occlusive dz w/ some systemic dz’s; ex sickle cell



    • Anomalous coronary artery: Rare; coronary arteries arise from opposite sinus of Valsalva increases risk for ischemia and sudden death



      • Usually p/w sudden death but 5/27 in 1 study w/ CP in prior 2 yr


      • Chest pain associated w/ exertion; often nml physical exam; usually silent or S3 and/or S4 (cardiac dysfunction)


      • EKG and stress test have not shown to be helpful in identifying at-risk pts


    • 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.


    • 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


    • Pulm HTN: Unclear mech; may be 2/2 pulm art stretch or RV ischemia. (Am Fam Physician 2001;63:1789)


    • Tachyarrhythmias: Abrupt onset and cessation, w/ or w/o activity, often w/ N/V.



      • Exam usually normal; EKG may demonstrate delta wave if pre-excitation (Wolf-Parkinson-White w/ bypass tract).


  • Idiopathic: 21% cases no cause identified in prospective study (Pediatrics 1988;82:319)



    • 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


  • Musculoskeletal: 15% cases in prospective study (Pediatrics 1988;82:319)

Jun 19, 2016 | Posted by in PEDIATRICS | Comments Off on Cardiology

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