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PEDIATRICS EXAM REVISION > CARDIOLOGY > Flashcards

CARDIOLOGY Flashcards

1
Q

What is the differential diagnosis of prolonged QT?

A
  1. Congenital: -Romano-Ward syndrome (most common genetic cause of prolonged QT syndrome, autosomal dominent) -Jervell-Lange-Nielsen syndrome (associated with deafness) 2. Acquired -Drugs (antiarrhythmics, dexmedetomidate, TCAs, antipsychotics, antibiotics such as macrolides) -Electrolytes (hypocalcemia, hypokalemia, hypomagnesemia) -Intracranial lesion (encephalitis, head trauma, stroke) -Cardiac disease
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2
Q

What is the treatment for myocarditis?

A

SUPPORTIVE for mild cases 1. Bed rest 2. Digoxin 3. Cautious diuresis since they’re preload dependent (will need some volume) 4. Afterload reduction - ACE inhibitor 5. Anti arrhythmic For severe cases: may need inotropes/ICU support

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3
Q

What is the rule of 1/3s for myocarditis?

A

1/3 complete recover 1/3 develop chronic dilated cardiomyopathy and require lifelong failure management 1/3 require transplant or have sudden death from arrhythmia

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4
Q

What is the differential diagnosis for left axis deviation on ECG (5)?

A

Left axis deviation is always abnormal 1. AVSD 2. Tricuspid atresia 3. Pulmonary atresia 4. Pulmonary stenosis 5. Single LV

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5
Q

What is the cause of biventricular hypertrophy on ECG?

A

VSD

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6
Q

What 3 congenital heart diseases is most likely to present with severe cyanosis within the first few hours of life?

A
  1. Transposition of the great arteries (MOST COMMON PRESENTING CYANOTIC LESION TO PRESENT IN NEWBORN PERIOD) -only mixing is through an open PDA and PFO -need PGE1 to keep PDA open in order to maintain oxygenation to systemic circulation
  2. Pulmonary atresia
  3. Ebstein’s anomaly
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7
Q

What are the clinical signs and symptoms of a “tet spell” (3)? What occurs physiologically during a “tet spell”?

A

(aka hypercyanotic spell)

  1. Acute onset of intense cyanosis
  2. Sudden softening of murmur (due to decreased blood flow through the obstructed right outflow tract)
  3. Deep rapid respiratory pattern (no work of breathing should be seen theoretically)

“Tet spell” - acute, sudden onset of increased right ventricular outflow tract obstruction and resultant decreased pulmonary blood flow (can be precipitated by agitation, fever, exercise, etc) –> obstruction of deoxygenated blood flow into the pulmonary artery –> deoxygenated blood shunts through the large VSD into the left ventricle –> deoxygenated blood flows into systemic circulation causing cyanosis -typically present starting at around 2 months of age as right ventricular outflow tract obstruction worsens -indication for urgent surgical repair

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8
Q

What are the 4 characteristic heart defects in Tetralogy of Fallot?

A
  1. Overriding aorta (empties from both the LV and RV) 2. RVH 3. Right ventricular outflow tract obstruction (ie. pulmonary stenosis) 4. VSD
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9
Q

In Tetralogy of Fallot, what does the severity of clinical signs and symptoms depend on?

A

The degree of right ventricular outflow tract obstruction

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10
Q

What 3 genetic conditions can be commonly be associated with Tetrology of Fallot?

A
  1. DiGeorge syndrome (22q11 deletion)
  2. Down syndrome
  3. Alagille syndrome
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11
Q

What is the immediate management of a “tet spell”?

A

Step-wise approach: if one step fails, move onto the next

  1. Put patient in knee-chest position -as with squatting, knee-chest position increases systemic vascular resistance, thus increasing left ventricular pressure and decreasing the right to left shunt of deoxygenated blood, promoting flow instead back into the lungs -also increases venous return to right side of heart to promote flow to lungs
  2. Administer O2 -O2 is pulmonary vasodilator (decreasing pulmonary vascular resistance and thus increases blood flow to lungs) and systemic vasoconstrictor
  3. Administer morphine (0.1 mg/kg) and give fluid bolus -morphine theoretically decreases agitation and thus RVOT obstruction -fluids improves venous return
  4. Administer IV beta blocker (propanolol 0.1 mg/kg) -causes relaxation of RVOT obstruction
  5. Administer IV phenylephrine (selective alpha agonist) -increases afterload (systemic vascular resistance)
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12
Q

What is a PVC?

A

Premature ventricular contraction - heartbeat is initiated by Purkinje fibers in the ventricles instead of the SA node -wide QRS -ventricles contract before atria has had time to fill them with blood

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13
Q

What are the 4 types of PVCs?

A
  1. Bigeminy -PVC occurs after every normal beat = non concerning
  2. Trigeminy -two normal beats to one PVC = non concerning 3. Quadrigeminy -three normal beats to one PVC = non concerning
  3. Ventricular tachycardia -3 or more PVCs occuring in a row = concerning obviously
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14
Q

What noninvasive tests can be ordered to investigate a history of arrhythmia (4)?

A
  1. ECG
  2. Holter monitor
  3. Event recorders -loop recorders: children always wear the device and press a button when they experience symptoms -pacer tracers: connected to telephone for recording
  4. ECHO
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15
Q

What are the two treatment modalities for chronic arrhythmias?

A
  1. Medical therapy with antiarrhythmics 2. Catheter ablation therapy
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16
Q

When would catheter ablation be the treatment of choice for a child with a tachyarrthymia over medical therapy?

A

If tachyarrhythmia has caused a life-threatening event

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17
Q

What is the treatment of choice for children with bradyarrythmias?

A

Cardiac pacing

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18
Q

What can be seen on ECG of a patient with Wolff-Parkinson-White syndrome (2)?

A
  1. Delta waves - short PR interval with upsloping, reflects pre-excitation (electrical conduction from atria to ventricle via pathway other than AV node) since the normal delay between the P and the R is missing (ie. the normal delay of electrical conduction by the AV node)
  2. Wide QRS
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19
Q

What are the 2 types of SVT (and 2 subtypes within each type)?

A

1. Re-entry

a) AVRT (atrioventricular reentrant tachycardia)
b) AVNRT (atrioventricular nodal reentrant tachycardia)
2. Automaticity: MAY see variability, warm up and slow down period, usually a bit lower rate, most will NOT respond to adenosine
a) Ectopic atrial tachycardia
b) J_unctional ectopic tachycardia (JET)_

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20
Q

What is Wolff-Parkinson-White Syndrome?

A

Pre-excitation syndrome: presence of abnormal accessory electrical conduction pathway (Bundle of Kent) between the atria and ventricles

  • pathway conducts electrical activity at higher rate than AV node and thus, if pt had atrial flutter, would conduct all the beats to the ventricles (bypassing the AV node’s natural ability to slow down atrial impulses to protect the ventricles from beating too fast)
  • risk of ventricular fibrillation and sudden death
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21
Q

Describe the pathophysiology of AVRT SVT.

A
  • presence of accessory pathway outside of AV node
  • normal SA antegrade conduction goes through the AV node and then retrograde up accessory pathway to reactivate the ventricles
  • in WPW, normal SA goes antegrade through the accessory pathway bypassing AV node (and thus no normal delay in conduction)
  • more likely in < 6 yo
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22
Q

Describe the pathophysiology of AVNRT SVT.

A
  • presence of 2 conducting pathways WITHIN the AV node (one fast and slow) creating a reentrant loop using one pathway in antegrade direction and one in retrograde
  • more likely in > 6 yo
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23
Q

Adenosine is only effective at terminating which type of SVT (2)?

A

Re-entry

  1. AVRT
  2. AVNRT

-Adenosine blocks AV node conduction

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24
Q

Why do vagal maneuvers assist in terminating SVTs?

A

Vagal maneuvers activate parasympathetic nervous system conducted to the heart by the vagus nerve

-increase AV nodal block to eliminate conduction to the ventricles

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25
Q

Which antiarrhythmics should be avoided in children with WPW (2)?

A
  1. Digoxin
  2. Calcium channel blockers (ie. verapamil) Both have potential proarrhythmia effects and can enhance conduction properties of accessory pathway (by blocking AV node so the impulse is forced to go to the accessory pathway) resulting in more rapid ventricular rate during atrial flutter and increased risk for sudden death
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26
Q

In which clinical circumstances do you worry that PVCs may lead to increased risk of sudden cardiac death/

A
  1. Post-op CHD
  2. Poor cardiac function (ie. cardiomyopathy)
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27
Q

What 5 features of syncope may be suggestive of a cardiogenic etiology?

A
  1. Sudden onset (“drop”) without prodromal symptoms or awareness
  2. Occurred during exercise or startle
  3. Limp or lifeless during syncope leading to injury
  4. Palpitations, chest pain or abnormal heart rate noted before event
  5. Family history of sudden death
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28
Q

What are 5 causes of cardiogenic syncope with risk of sudden cardiac arrest?

A
  1. HOCM
  2. Arryhthmia:
    a. WPW
    b. Prolonged QT syndrome
    c. Arrhythmogenic RV dysplasia
  3. Coronary artery anomalies ALPCA (ie. coronaries comes between pulmonary artery and aorta; during exercise, increases stroke volume and thus great vessel size and squishes coronary arteries and get MI)
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29
Q

What 3 congenital heart defects are seen with maternal diabetes?

A
  1. VSD 2. HOCM 3. PDA
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30
Q

Which cyanotic heart defect is most likely to present in: -newborn period -infancy period -childhood period

A
  • Newborn period: transposition of great arteries
  • Infancy period: tricuspid atresia
  • Childhood period: TOF
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31
Q

What is Ebstein’s anomaly?

A

Abnormal tricuspid valve leaflets (either abnormal shape, too large or adhered to the septum) -get constant connection between RA and RV with tricuspid regurgitation due to inadequate valve closure -wall to wall heart on CXR

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32
Q

When interpreting an ECG in a patient with a pacemaker, what does it mean to have “good capture”?

A

Should always check for good capture on an ECG in a patient with a pacemaker: -means that every time the pacemaker discharges (“spike” on ECG), there should be a subsequent QRS following each “spike”

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33
Q

What is the sequence of reading an ECG?

A
  1. Heart rate 2. Rhythm -Sinus: P before every QRS, upright P in leads II, III, and AVF 3. Axis -Look at lead I and AVL: upright? -Look at II, III, and AVF: upright? (overall: leads II, III and AVF are stickers on legs so if you see upright QRS, means that electrical impulse is moving towards the stickers on legs from above ie. the SA node so this means this is atrial impulse. If you see inverted QRS, means that the electrical impulse is coming from the ventricles moving away from the legs) 4. Look at PR and QRS intervals and compare to normal for age values 5. Look at precordial leads (V1-V6) for normal R wave progression -QRS should get bigger as you move from V1-V6 (since in older children, left ventricle is thicker than right ventricle so higher voltage) 6. Look at T wave in all leads -should always be upright in limb leads -in children < 10 yo, normal to have inverted T waves in V1-V6 -in children > 10 yo, should start to have upright T waves starting in V6 and moving towards V1 (can take up to 18 yo for T wave to become upright in all V1-V6 leads) 7. QTc calculation and compare to normal for age
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34
Q

What clinical features are seen in DiGeorge Syndrome?

A

CATCH-22 Deletion of chromosome 22q11

  1. Congenital heart defect (usually TOF)
  2. Abnormal facies
  3. Thymic aplasia
  4. Cleft palate
  5. Hypocalcemia
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35
Q

What are 2 things you MUST do prior to cardioverting an infant presenting with new SVT?

A

Since we don’t know how long infant has been in SVT for, may have developed heart failure or poor cardiac function; thus, may be rate dependent for cardiac output. With cardioversion and return to normal HR, may significantly decrease cardiac output and thus cause them to go into cardiogenic shock.

  1. Need to call Cardiology and PICU and be prepared for this circumstance in order to do cardioversion in controlled setting
  2. Need to put a 12 lead ECG or rhythm monitor on the patient
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36
Q

What is Beck’s triad?

A

Clinical features of cardiac tamponade:

  1. Hypotension
  2. Muffled heart sounds
  3. Distended neck veins
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37
Q

What is the underlying mutation in prolonged QT syndrome?

A

Mutations in cardiac potassium and sodium channels = ion channelopathies

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38
Q

What is the most common presenting symptom of LQTS in children?

A

Syncopal episode brought on by exercise, fright, or sudden startle -some occur during sleep (LQT type 3)

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39
Q

What is QTc? -What QTc is considered prolonged?

A

-QTc = QT interval (ventricular depolarization and repolarization) that is adjusted for heart rate differences -Prolonged = > 0. 440 (in infants < 6 mo, QTc up to 0.490 may be normal)

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40
Q

What is the significance of genetic testing in identifying prolonged QT syndrome?

A

Genotyping can identify mutation in ~75% of patients known to have LQTS by clinical criteria. -if negative, it does NOT mean that a patient does not have LQTS if they fit clinical criteria BUT it does help identify asymptomatic affected relatives of the index case

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41
Q

What is the treatment for prolonged QT syndrome?

A
  1. Beta blockers -if beta blockers cause significant bradycardia, may need pacemaker
  2. For patients who have had cardiac arrest, need implantable cardiac defibrillator (ICD)
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42
Q

What other ECG features can be seen in prolonged QT syndrome? (3) -what are patients with prolonged QT syndrome at risk for? (2)

A
  1. Bradycardia
  2. Notched T waves
  3. T wave alternans (alternating upright and downgoing T waves)
    - At risk for torsades de pointes and ventricular fibrillation
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43
Q

What is the underlying pathophysiology of Hypoplastic Left Heart Syndrome?

-how does circulation occur? -main problems resulting from abnormal circulation?

A
  1. Hypoplasia of left ventricle (secondary to atresia of the mitral orifice)
  2. Hypoplasia of ascending aorta (secondary to atresia of the aortic ortifice) **Remember: no flow, no grow

*Circulation: red blood (100% O2) from lungs –> LA cannot pass to LV and aorta –> passes through PFO or ASD –> RA and mixes with blue blood (60%) from SVC/IVC = 85% O2 –> RV –> pulmonary artery –> lungs and systemic circulation via PDA to descending aorta with blood flow retrograde to ascending aorta (to supply cerebral and upper extremity perfusion) and coronary arteries

-main problems:

  1. Increased pulmonary flow (from moderate or large ASD and all blood flowing into RA –> RV –> lungs)
  2. Pulmonary vein hypertension (from small ASD or restrictive PFO leading to backup of blood in LA and pulmonary vein)
  3. Inadequate maintenance of systemic circulation
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44
Q

What are the clinical features of hypoplastic left heart syndrome? (3)

A
  1. Increased pulmonary flow: can have pulmonary edema (crackles, wet lungs on CXR)
  2. Decreased systemic circulation: weak or absent pulses, cyanosis, shock once PDA starts closing
  3. Right ventricular volume overload: right ventricular parasternal lift

**typically present within 1st few hours or days of life

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45
Q

What 3 genetic syndromes can HLHS be seen in?

A

T, T, T

  1. Turners
  2. Trisomy 13
  3. Trisomy 18
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46
Q

What is seen on ECG of patients with HLHS?

A
  1. Right ventricular hypertrophy (due to volume overload)
  2. Prominent P waves (right atrial dilatation from volume overload)
  3. Reduced left sided signals
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47
Q

What is the association of central nervous system abnormalities with HLHS? -association of dysmorphic features?

A

30% of HLHS have major or minor central nervous system abnormalities

  • 40% of HLHS have dysmorphic features
  • thus, need genetics, neuro, ophtho assessment before surgery
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48
Q

What is the treatment for HLHS?

A
  1. Prostaglandin E1 to maintain PDA
  2. If ASD small- do catheter based septostomy
  3. manage pulmonary overload with diuretics
  4. Norwood procedure within 1st week…then eventually a Fontan
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49
Q

Describe the Norwood procedure. -stage 1 (commonly called the Norwood) -stage 2 -stage 3

A

Stage 1 (neonatal period): commonly referred to as the Norwood -atrial septectomy -attach the proximal pulmonary artery to the hypoplastic aortic arch with a patch to form a neoaorta to supply systemic circulation -Blalock-Taussig shunt connects the subclavian artery to the main pulmonary artery to increase total pulmonary blood flow and thus increases oxygen saturation to systemic circulation (decreases cyanosis) Stage 2 (2-6 mo of age): Glenn anastomosis -disconnect the SVC from the RA and connect it directly to the pulmonary arteries Stage 3 (2-3 yr of age: modified Fontan procedure -disconnect the IVC from the RA and connect it directly to the pulmonary arteries

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50
Q

Describe the circulation in HLHS post Norwood procedure.

A

Blue blood from SVC/IVC enters pulmonary artery directly –> passive flow to lungs –> LA –> ASD –> RA –> RV –> pulmonary artery –> neoaorta to systemic circulation

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51
Q

What are the common ductal-dependent cardiac lesions? -ductal dependent pulmonary blood flow (4)

-ductal dependent systemic blood flow (3)

A

Ductal dependent pulmonary blood flow:

  1. Critical pulmonary valve stenosis
  2. Pulmonary atresia
  3. TOF with severe pulmonary stenosis
  4. Tricuspid atresia with pulmonary stenosis or pulmonary atresia

Ductal dependent systemic blood flow:

  1. Coarctation of the aorta
  2. Hypoplastic left heart syndrome
  3. Interrupted aortic arch
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52
Q

What is the distribution of aortic stenosis in males vs. females?

A

More common in males (3:1)

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53
Q

What is the most common form of aortic stenosis and what is the pathophysiology?

A

Most common form: valvular aortic stenosis

-thickened aortic leaflets and commissures are fused -obstruction to LV blood flow = increased LV systolic pressure = LVH

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54
Q

What is the triad of Shone syndrome?

A
  1. Subvalvular aortic stenosis 2. Mitral stenosis 3. Coarctation of aorta
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55
Q

What are clinical features of Williams syndrome? (7) -what is the underlying genetic mutation?

A
  1. Supravalvular aortic stenosis 2. Developmental delay 3. Hypercalcemia 4. Elf face (prominent lips, abnormal teeth) 5. Hypothyroidism 6. Cocktail party personality 7. Joint hypermobility Genetic mutation: chromosome 7q11.23 (codes for elastin protein) Williams loves going to 7/11 to drink slurpees and socialize with his big lips
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56
Q

What are the clinical features of aortic stenosis? -murmur?

A

Think decreased left ventricular outtract flow and back up of blood into LA and lungs! -decreased cardiac output = decreased pulses, decreased urine output -left ventricular failure and pulmonary edema -murmur: early systolic ejection click at apex and left sternal edge with RUSB murmur radiating to neck (aortic arch)

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57
Q

What are findings on ECG of aortic stenosis?

A
  1. LVH 2. left heart strain (inverted T waves in left precordial leads)
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58
Q

What is the treatment for aortic stenosis? -what is a complication of untreated severe aortic stenosis?

A

Balloon valvuloplasty or surgery -untreated severe AS: sudden cardiac death especially during exercise

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59
Q

What are patients with bicuspid aortic valves at increased risk for developing?

A

Dilated ascending aorta -dissection and rupture are described in adult populations due to severe aortic root dilation but there is insufficient data to determine the risk in children (only isolated cases reported)

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60
Q

What is the triad of Holt-Oram syndrome?

A
  1. Hypoplastic or absent radii 2. 1st degree heart block 3. ASD
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61
Q

What is the difference between an ostium primum and ostium secundum?

A

Both are types of ASDs -ostium primum: defect is at center of the septum -ostium secundum: defect is inferior and is part of an AV canal defect and can involve tricuspid or mitral valve abnormalities

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62
Q

How do children with VSDs typically present? -large vs. small

A

Large VSD: signs of CHF usually appear at 4-8 wks of age when the pulmonary vascular resistance drops and pulmonary blood flow increases from L-R shunting Small VSD: spontaneous closure often occurs

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63
Q

What is the indication for closure of ASD? -when does it occur?

A

Secundum ASD associated with RV dilation (from volume overload) and increased pulmonary blood flow -repair occurs electively at 3-5 years of age

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64
Q

What are the clinical features of ASD?

A

Most children are asymptomatic -when they do have symptoms, you hear a fixed split S2

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65
Q

Why do you hear a fixed split S2 in ASD?

A

From RV volume overload and prolonged ejection of blood during systole leading to delayed pulmonary valve closure

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66
Q

What is the result of persistent increased pulmonary blood flow?

A

Pulmonary HTN

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67
Q

What is the pathophysiology behind congestive heart failure due to left to right shunting? -Eisenmenger

A
  1. Resp symptoms due to increased pulmonary blood flow and pulmonary edema 2. Increased left ventricular output since cardiac output to systemic circulation is decreased due to loss through the L to R shunt –> to maintain this output, have increased heart rate and stroke volume –> increased sympathetic nervous system activity –> increased catecholamines –> increased total body oxygen consumption, sweating, irritability and FTT –> remodeling of heart with dilatation and hypertrophy –> Eisenmenger (pulmonary hypertension with reversal of shunt from R-L)
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68
Q

What are characteristics of Still murmur? -location & quality -age group

A

Classic vibratory murmur -LLSB and apex -low-frequency vibratory “twanging string” -3-6 yo -turbulent flow out of LV -decreases in intensity with sitting

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69
Q

What are the characteristics of a pulmonary ejection murmur? -location & quality -age group

A

-ULSB -early to midsystolic murmur -crescendo-decrescendo -8-14 yo -from turbulence of blood flow into the pulmonary vein

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70
Q

What are the characteristics of a pulmonary flow murmur of newborn? (PPS) -location & quality -age group

A

-ULSB -transmits to axilla and back -premature and full-term newborns -disappears by 3-6 months of age -angulation or narrowing of peripheral pulmonary stenosis -heard usually during resolving URTI

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71
Q

What are the characteristics of a venous hum murmur? -location & quality -age group

A

Continuous, supraclavicular murmur -3-6 years old -from turbulence of flow in jugular venous system HENCE why you hear it best in the supraclavicular area -can decrease it by turning neck or compressing the jugular venous system in the neck *****ONLY INNOCENT MURMUR THAT WILL INCREASE WITH SITTING

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72
Q

What are the characteristics of a carotid bruit murmur?

A

Right supraclavicular areas and over carotids -any age

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73
Q

What does sitting up do to: -venous hum murmur -Still’s murmur

A

Venous hum: increases with sitting up Still’s: decreases with sitting up

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74
Q

What is the most common innocent murmur?

A

Still’s murmur = medium pitched, vibratory or musical systolic ejection murmur heard at the LLSB

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75
Q

What is pulsus alternans?

A

Pulsus alternans: beat to beat variability of pulse strength due to decreased left ventricular performance -seen in severe CHF

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76
Q

Describe the pathophysiology of pulsus paradoxus.

A

Fall in SBP > 10 mm Hg during inspiration -NORMALLY: when you take a breath, you increase intrathoracic negative pressure and increase venous return to the right side of the heart and lungs = this causes blood pooling in the lungs and thus decreased pulmonary venous blood flow = decreased blood return to LA = decreased cardiac output = SBP drops by no more than 10 mm Hg. Also more right heart filling impairs left heart filling and decreased stroke volume -IN PULSUS PARADOXUS: pressure is equalized between right heart and left heart = when right heart fills, pushes septum into left side of heart impairing filling since left heart cannot expand to accommodate blood flow with the constriction) = decreased stroke volume = drop in SBP > 10 mm Hg. Also can have increased negative thoracic pressure exerting a transmural load onto the LV and thus increases afterload, decreasing stroke volume

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77
Q

What are causes of pulsus paradoxus? (4)

A
  1. Pericardial tamponade 2. Constrictive pericarditis 3. Severe respiratory disease (status asthmaticus, pneumonia) 4. Myocardium diseases that affects wall compliance (amyloidosis)
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78
Q

What is the antidote for digoxin toxicity? -what if digibind is not available?

A

Digibind = digoxin-specific Fab antibody fragments = binds free digoxin in intravascular and interstitial space that forms inactive complex and then you pee it out -if not available, can use phenytoin or lidocaine to stabilize the myocardium and decrease ventricular irritability -atropine is helpful too -also use activated charcoal

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79
Q

How does Digoxin work? What are the signs and symptoms of digoxin toxicity? (5)

A

-Digoxin blocks the Na-K-ATPase pump = leads to movement of K from intracellular to extracellular and movement of Na and Ca into cells -increase of Ca in cardiac myocardial cells improves inotropy. Also decreases nodal conduction Digoxin toxicity: -bradycardia & heart block -nausea and vomiting -lethargy, confusion and weakness -HYPERKALEMIA!!!!! This is a big one! -pulsus bigeminus (2 heart beats close together followed by long pause)

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80
Q

Why should digoxin NEVER be given in WPW patient?

A

Digoxin decreases AV nodal conduction BUT can enhance cnoduction through a bypass tract THUS increasing chance of ventricular fibrillation

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81
Q

What connective tissue diseases may be associated with mitral valve prolapse? (3)

A
  1. Marfan syndrome 2. Ehlers-Danlos syndrome 3. Osteogenesis imperfecta
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82
Q

What is mitral valve prolapse? -physical exam finding? -treatment?

A

Abnormal mitral valve mechanism that causes billowing of one or both mitral valve leaflets into the LA at the end of systole -physical exam finding: apical murmur with a click -Minimal mitral valve prolapse can be a normal variant -Treatment: nothing!

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83
Q

What conditions are associated with the development of myocarditis? (3 broad classes)

A
  1. Infectious -bacterial: diphtheria, strep species, mycoplasma -viral: Coxsackie B (most common), HIV, echoviruses, rubella, adenovirus -fungal -protozoal: trypanosomiasis (Chagas disease), toxoplasmosis 2. Inflammatory -Kawasaki -SLE -RA -IBD 3. Chemical and physical agents -doxorubicin -radiation injury -lead -alcohol
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84
Q

What is Chagas disease? -clinical features (2) -what is Romana sign?

A

American trypanosomiasis infection -Romana sign (unilateral, painless, violaceous, palpebral edema accompanied by conjunctivitis) + CHF

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85
Q

What are the causes of a single S2? (6)

A

-Physical presence of only one semilunar valve: 1. Aortic atresia 2. Pulmonary atresia 3. Truncus arteriosus -P2 not audible: 4. Tetralogy of fallot (pulmonary stenosis) 5. Transposition of great arteries -A2 delayed: 6. Severe aortic stenosis

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86
Q

What is the cause of a loud P2?

A

Pulmonary hypertension since pulmonary valve is closing against pressure

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87
Q

Name the 4 cyanotic CHD with increased pulmonary blood flow?

A

-Single ventricle pathology 1. HLHS 2. Truncus arteriosus 3. Transposition of the great vessels 4. TAPVR without obstruction ***These cause cyanosis because of systemic and venous blood mixing

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88
Q

Name the 4 cyanotic CHD with decreased pulmonary blood flow?

A
  1. TOF 2. Pulmonary atresia 3. Tricuspid atresia 4. TAPVR ***These cause cyanosis because of obstruction to pulmonary blood flow
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89
Q

What syndrome is associated with pulmonary stenosis and hypercholesterolemia?

A

Alagille syndrome (hypercholesterolemia is secondary to liver disease)

90
Q

What evaluations can be done if a vascular ring is suspected? (5)

A
  1. CXR: to identify right sided aortic arch 2. Barium swallow: was the gold standard; confirms external indentation of esophagus in 95% of cases 3. MRI: noninvasive and is the primary diagnostic modality 4. Arteriogram: rarely used 5. Echocardiogram: cannot identify the ring itself but can rule out congenital heart lesions which can occur simultaneously
91
Q

What is commotio cordis?

A

Ventricular fibrillation due to a blunt, non-penetrating direct blow to the chest during the vulnerable phase of repolarization

92
Q

What percentage of HOCM is genetically inherited? -what is the inheritance pattern?

A

60% of HOCM is genetic -AD

93
Q

What are the 4 common causes of AV block?

A
  1. Myocarditis 2. Maternal history of lupus 3. Lyme disease 4. Acute rheumatic fever
94
Q

What cardiac defect is associated with maternal lithium use?

A

Ebstein’s anomaly

95
Q

What are the features of VACTERL syndrome?

A

Vertebral anomalies Anal atresia Cardiac defects TEF Renal agenesis/dysplasia Limb defects

96
Q

What cardiac condition is associated with bilateral rib notching?

A

Coarctation of the aorta = due to collateral vessels forming around the ribs impairing bone growth

97
Q

Name two cardiac conditions in which a decrease or disappearance of a murmur is BAD NEWS BEARS.

A
  1. Tetralogy of fallot: indicates worsening RV outflow tract obstruction 2. VSD: indicates that Eisenmenger syndrome has developed with increased pulmonary vascular resistance and thus reversal of shunt from R to L
98
Q

What are the ECG findings of hypokalemia? (3)

A
  1. Prominent U wave (small deflection immediately following the T wave 2. Inverted T wave 3. Depressed ST segment
99
Q

What are the ECG findings of hyperkalemia? (4)

A
  1. Prolonged PR interval 2. Wide QRS 3. Tall, peaked T waves 4. Sinusoidal wave
100
Q

What is the definition of torsades de pointes?

A

Polymorphic ventricular tachycardia with a prolonged QT interval

101
Q

What vagal maneuvers can be used to treat SVT in infants? (2)

A
  1. Ice in bag over face 2. Gagging with tongue depressor ***Do NOT use ocular pressure as it has been associated with retinal damage
102
Q

What are the two types of familial hypercholesterolemia? -pathophysiology? -features of each? -bloodwork findings?

A

Lack of LDL receptors on cell membrane so no negative feedback loop to stop cholesterol production 1. Homozygous -xanthomas at < 10 yo -vascular disease < 20 yo -extremely rare (1 in 1 million) 2. Heterozygous -less likely to have clinical features -more common (1 in 500) -increased LDL -increased cholesterol

103
Q

Who should be checked for elevated cholesterol levels?

A

2-10 year old: 1. Family history (parent or grandparent) with age < 55 with premature cardiovascular disease 2. Parent with high cholesterol 3. Unknown family history 4. Children with risk factors: -Overweight (BMI 85-95%) -Obese (BMI >95%) -Diabetes -Hypertension > 95th percentile -Smokers -nephrotic syndrome

104
Q

What is the management of hypercholesterolemia?

A
  1. Lifestyle + diet modification x 6 months, then recheck -not a lot of research on pharmaceutical therapy on treating hypercholesterolemia in children 2. Statins: do not start if < 8 yo
105
Q

What bloodwork should you monitor while patients are on statins? (2)

A
  1. Liver enzymes 2. CK
106
Q

What are cardiac causes of SVT? (4)

A
  1. Post op cardiac 2. Ebstein’s anomaly 3. Cardiomyopathy 4. Myocarditis
107
Q

What is the lethal arrhythmia of WPW syndrome?

A

Atrial fibrillation which then travels down the bundle of kent accessory pathway with a rapid ventricular response leading to ventricular fibrillation

108
Q

What is the most common cause of SVT in children?

A

WPW syndrome

109
Q

What are Osler nodes? What are Janeway lesions?

A

Osler nodes: PAINFUL nodules on pads of fingers and toes in IE due to immune complex deposition Janeway lesions: PAINLESS, hemorrhagic nodular lesions on palms and soles in IE due to septic emboli Osler is a dude so he’s whiney when it comes to pain

110
Q

What are the signs of pericarditis on exam?

A

Friction rub, distended neck veins, hepatomegaly, pulsus paradoxus, muffled heart sounds

111
Q

What is the most important complication of untreated Kawasaki disease?

A

Coronary artery aneurysms –> heal with stenosis –> MI

112
Q

What is the typical age of children with Kawasaki disease?

A

6 mo - 5 yr -however, can also happen in infants and teenagers (higher risk of developing coronary artery aneurysms, possible because of delayed diagnosis)

113
Q

What condition should be suspected if you see a child with fever for 5 days and marked erythema/induration around BCG scar?

A

Kawasaki = early, specific marker

114
Q

What is the medical management of Kawasaki disease?

A
  1. IVIG: decreases incidence of coronary artery aneurysms -single infusion over 8-12 hrs of 2 g/kg -if still febrile > 36 hr after first infusion, can give second infusion of 2 g/kg 2. High dose aspirin (80 mg/kg div q6h) (decreases fever and discomfort, unclear whether it decreases coronary artery aneurysms) until fever free x 48 hrs, then switch to low dose aspirin (3 mg/kg/d) x 6-8 wks until f/u ECHO (decreases thrombotic complications). -If ECHO normal, d/c. If ECHO abnormal, then continue indefinitely.
115
Q

What is the likelihood of developing coronary artery aneurysms with untreated vs. treated Kawasaki disease?

A

Untreated: 25% Treated: < 5%

116
Q

What are the indications for prostaglandin E1 in the neonate?

A
  1. Inadequate pulmonary blood flow: -Pulmonary atresia with intact ventricular septum -Tricuspid atresia with intact ventricular septum -critical pulmonary stenosis 2. Inadequate systemic blood flow: -HLHS -interrupted aortic arch -Critical coarc of aorta 3. Inadequate mixing -TGA
117
Q

What are the actions of the following receptors: -alpha receptors -beta 1 receptors -beta 2 receptors -dopaminergic receptors

A

-alpha receptors: vascular smooth muscle vasoconstriction -beta 1 receptors: myocardial smooth muscle inotropy and chronotropy -beta 2 receptors: vascular smooth muscle vasodilation (bronchodilation) -dopaminergic: renal and mesenteric vascular smooth muscle vasodilation

118
Q

What are 2 common rhythm disturbances after the Fontan procedure?

A

Fontan procedure involves manipulation of the RA 1. Loss of sinus rhythm –> nonsinus atrial rhythm or junctional rhythm 2. Intra-atrial reentrant tachycardia

119
Q

What is the most common form of ASD?

A

Ostium secundum

120
Q

What are the findings on ECG of ASD?

A
  1. Right axis deviation 2. RVH 3. RSR prime
121
Q

What are the indications for indomethacin in treating PDA? (3) -dose? What are the contraindications for indomethacin in treating PDA? (7)

A

Indications: 1. Deteriorating respiratory status 2. Poor cardiac output 3. Evidence of CHF -dose: indomethacin 0.1 mg/kg/day x 6 days Contraindications: 1. Thrombocytopenia 2. Renal impairment 3. Active bleeding (GI or intracranial) 4. Proven or suspected untreated infection 5. NEC or suspected NEC 6. Evidence of bleeding diathesis 7. CHD in which PDA is needed for pulmonary or systemic blood flow

122
Q

What are the side effects of indomethacin?

A
  1. Renal impairment 2. Platelet dysfunction 3. Pulmonary hemorrhage 4. GI hemorrhage 5. Hyponatremia 6. Hypoglycemia 7. Hyperkalemia (due to decreased renal function)
123
Q

What are 3 CXR findings of coarctation of the aorta?

A
  1. Rib notching 2. Intrapulmonary vascular markings increased 3. 3-sign on left para mediastinal shadow -prominent aortic bulge, indentation of descending aorta, post stenotic dilation of aorta
124
Q

What is the most common cardiac defect associated with Noonan syndrome and Alagille syndrome?

A

Pulmonary stenosis

125
Q

What congenital heart defect is most commonly seen with congenital rubella syndrome?

A

Peripheral pulmonary stenosis (of the pulmonary arteries leading to restricted bloodflow to lungs)

126
Q

What is the differential diagnosis of intracranial bruit? (9)

A
  1. Fever 2. Cardiac murmur 3. Intracerebral tumor 4. Thyrotoxicosis 5. Cerebral aneurysm 6. Increased ICP 7. Anemia 8. AV malformation (ie. vein of galen) 9. Meningitis
127
Q

What is the most common cardiac finding in IDM? -treatment

A

Septal hypertrophy with possible left ventricular outflow obstruction -resolves spontaneously within 1 year -usually requires no treatment -may need beta blockers if severe left ventricular outflow obstruction

128
Q

What is the vein of galen AVM? -associated with? (2)

A

Blood is shunted from arterial vasculature into venous system so you get high output heart failure -associated with heart failure & hydrocephalus

129
Q

What cardiac defect is a common cause of infective endocarditis in the Western world?

A

Mitral valve prolapse -but do NOT need prophylaxis because incidence of infective endocarditis is so low and mitral valve prolapse incidence is low

130
Q

What is the most common type of cardiomyopathy caused by doxorubin? -mortality risk?

A

Dilated cardiomyopathy -dose dependent -more likely to have cardiac damage if they have radiation treatment at the same time -mortality risk if heart failure develops: 30-50% -develops chronically (over months-years)

131
Q

What are ECG findings of anorexia nervosa?

A
  1. Bradycardia 2. Low voltages 3. Prolonged QT 4. Wide QRS
132
Q

Where is the most common location of coarctation of aorta?

A

Juxtaductal (right beside PDA, below the origin of the left subclavian artery)

133
Q

What are the Duke’s Criteria for infective endocarditis?

A

Definite diagnosis: 1. Intracardiac or embolized vegetations on histology Possible diagnosis: Need 2 major, 1 major + 3 minor or 5 minor Major: 1. 2 positive blood cultures 2. Evidence of endocardial involvement: positive echo for vegetations OR new regurg murmur Minor: -predisposition: 1. Predisposition: predisposing heart condition OR IV drug use 2. Fever 3. Vascular phenomena: septic emboli to lungs, intracranial hemorrhage, conjunctival hemorrhages, janeway lesions 4. Immunologic phenomena: glomerulonephritis, Roth spots, Osler’s nodes, positive RF 5. Microbiological evidence: positive blood culture x 1 or of organism not known to cause IE 6. Echocardiographic findings: consistent with IE but does not meet major criterion as noted above

134
Q

What organisms most commonly cause infective endocarditis? (4) -what empiric abx would you start in a patient with suspected IE? -treatment duration

A
  1. Strep viridans 2. Staph aureus 3. Staph epi 4. H flu

ANTIBIOTICS: -start Amp + Gent

-treatment duration 4-6 wks

135
Q

What are three causes of congenital heart block?

A
  1. Maternal lupus 2. Sjogren’s syndrome 3. Myocardial tumors
136
Q

What is Pompe’s disease? -how is it inherited? -clinical features? -lab findings?

A

Glycogen storage disease -glycogen accumulates in cardiac, smooth muscle, and skeletal muscle -autosomal recessive -Presents with severe hypotonia, cardiomegaly & heart failure, feeding difficulties, constipation, hepatomegaly -lab findings: elevated CK, LDH, AST

137
Q

What ECG findings are found in Pompe’s disease? -CXR finding?

A
  1. High voltage QRS due to ventricular hypertrophy 2. Shortened PR CXR: ECG finding
138
Q

What are anesthesia considerations in pre-op assessment of Down Syndrome patient? (6)

A
  1. Atlantoaxial instability: consider in intubation, order flex-ex views before intubation 2. Large tongue: difficult airway 3. Risk of post op resp infections 4. Congenital cardiac lesions: if repaired, increased risk of arrhythmias post-op 5. Pulmonary hypertension 6. OSA
139
Q

What is a cardiac condition that needs to be ruled out in every patient who has hypertension?

A

Coarctation of aorta

140
Q

In what condition do you see radio-femoral delay? -what is the cause?

A

Radio-femoral delay: seen in coarctation of aorta -normally, femoral pulse comes before radial pulse; however, it is reversed in coarc of aorta since femoral pulse is generated by collaterals which takes longer than the generation of radial pulse by large vessels

141
Q

In a patient with coarc of aorta, what does the presence of a systolic ejection click or thrill in the suprasternal notch suggest?

A

Bicuspid aortic valve (present in 70% of coarc cases)

142
Q

What is the underlying primary defect in tetralogy of fallot leading to the classic 4 findings?

A

Anterior deviation of the infundibular septum (conus) -allows for the VSD to happen since septum can’t grow up towards the conus -anterior deviation pulls the aorta forward giving the overarching aorta -spasm of the excess muscle causing the anterior deviation leads to tet spell

143
Q

Why might a baby with TOF suddenly deteriorate at 7 days of life? -what treatment should be started immediately?

A

If their right ventricular outflow tract obstruction is severe, their PDA may be their only means of pulmonary blood flow -at 7 days, the PDA closes, thus causing them to go into cardiogenic shock -treatment: PGE1

144
Q

What is the corrective surgical therapy for tetralogy of fallot?

A
  1. Relief of RV outflow tract obstruction - resection of obstructive muscle bundles 2. Patch closure of VSD 3. Pulmonary valvotomy (if pulmonary valve is stenotic) or valvectomy (if pulmonary valve is thickened or too small = add in a transannular patch) -valvotomy = leads to pulmonary insufficiency -now we aim to leave as much of the pulmonary stenosis as we can to prevent backflow but add in a patch to allow good forward flow 2nd option (less preferred): BT shunt
145
Q

What is an alternate way of obtaining a BP if you are getting an inaccurate one from the monitor?

A

Doppler BP! (can only get SBP from it however since the doppler is so sensitive, you will still hear the pulse down to pressure of 0 so won’t be able to obtain DBP)

146
Q

How do you check for RV enlargement in a neonate?

A

Put your thumb under the xiphoid process - should not feel any pulse if RV is normal. If RV enlarged, will feel a pulse

147
Q

What is considered a pre/pos ducal sat differential?

A

>10% is abnormal

148
Q

What is the hyperoxic test?

A
  1. Draw ABG on RA, expect PAO2 = 80-100 mm Hg; if PAO2 < 25 mmHg with normal PCO2 definite cardiac disease 2. then give 100% FiO2 for 5-10 minutes, draw another ABG from right radial artery. If PAO2 < 150 mm Hg, then cardiac disease for sure. If it goes up > 150 then it is likely not cardiac disease. ****Really, it is the lack of change with 100% O2 that indicates cardiac disease
149
Q

You have an unwell 2 mo baby with cyanosis and a CXR showing small heart and extremely wet lungs. What is your diagnosis?

A

Obstructed TAPVD -blood is trying to get back to the heart through a small vessel and into RA. If PFO is open, bloodflow will go from RA to LA to LV to body. If PFO closes, then you’re screwed

150
Q

Difference in CXR findings between obstructed TAPVR vs. unobstructed TAPVR?

A

Obstructed (obstructed flow into the heart): small heart, very wet lungs (looks reticular, like RDS) Unobstructed (L to R shunt): snowman sign, enlarged heart

151
Q

What is the classic finding of coarctation of aorta in neonate on ECG? -in children?

A

-in neonates: RVH on ECG since it is the right heart that’s been pumping through the PDA against the coarctation -in children: LVH on ECG since it’s the left heart that’s pumping against the coarctation

152
Q

What is the starting dose of PGE1? -other management with starting PGE1?

A

Start high at 0.2 mcg/kg/minute IV -Give a fluid bolus 20 cc/kg prior to prevent hypotension, run TFI at 130-150 cc/kg/d -Best to leave baby free breathing if stablized from above. Intubate if severely acidotic

153
Q

What is the most common type of VSD?

A

Perimembranous (70%)

154
Q

When is surgical correction indicated in VSD?

A

When there is no weight gain

155
Q

What are the V4R and V3R for on ECG?

A

V4R, V3R = look at right sided pathology

156
Q

What is the fast way to access rate on ECG?

A

300, 150, 100, 75, 60, 50 for each big box (5 little boxes)

157
Q

What are the criteria for sinus rhythm? (2)

A
  1. P for every QRS and QRS for ever P 2. Normal P axis
158
Q

At what age does RAD disappear on ECG?

A

After 6 months

159
Q

What does tall P wave on ECG signify? What about wide P wave or bifid?

A

Tall = right atrial enlargement Wide or bifid = left atrial enlargement

160
Q

What is the treatment for first degree AV block?

A

Nothing - usually asymptomatic, seen in athletes, anorexia nervosa

161
Q

What are 4 potential causes of third degree (complete) AV block?

A

Myocarditis, lyme disease, congenital, cardiac surgery

162
Q

Which leads should you see Q waves?

A

Q waves = septal depolarizaion -should be in the leads that look left (V5-V6) and leads that look down (II, III) -abnormal if absent in the expected leads or presence in other leads -common in African American population

163
Q

What is the difference between complete vs. incomplete RBBB? -what is the significance of the LBBB?

A

Complete = > 3 small squares = common in post op cardiac paients Incomplete = < 3 small squares = not clinically significant LBBB = very uncommon and usually indicates underlying pathology (ischemia)

164
Q

What is the normal QTC in males vs. females?

A

QTC < 440 msec in males QTC < 460 msec in females ***as QTc increases (>500 msec), the risk of arrhythmias increases dramatically

165
Q

What are 2 signs on ECG of acute pericarditis?

A
  1. Depression of PR interval 2. Diffuse ST elevation
166
Q

What does it mean if you have normal V1 and V6 but deep or tall V2-V4?

A

Nothing. This is normal in children

167
Q

What are ECG findings of LVH?

A
  1. ST depression or T wave inversion in V5-7 2. S wave in V1 > 95h percentile for age 3. R wave in V6 > 95th percentile for age 4. Deep Q waves in V5-7
168
Q

What is a possible cause of myocardial ischemia in a young child?

A

Anomalous left coronary artery from the pulmonary artery = see biventricular hypertropy, Q wave in V6, ST elevation

169
Q

Which CHD are essentially normal children post-op (and thus we do not need to call cardio if these children present in ED)? (5)

A

No exercise restrictions, no limitations, they are essentially a normal child 1. VSD 2. ASD 3. AVSD 4. TAPVD 5. Coarctation ***Only care if there are residual lesions

170
Q

Which post-op CHD should we worry about if they present to ED (and thus call cardio)?

A

Degree of worry is based on residual defect: 1. TOF 2. TGA 3. HLHS Essentially, worry MOST about Norwood, Glenn, Fontan, PA/VSD/MAPCAs (multiple aortopulmonary collaterals) = call cardio always if these patients come in for anything Anytime you hear “single ventricle physiology”, worry and call cardio! ***Call cardio and say “reassure me that I’ve done all the work-up”

171
Q

Why do we worry about children with a transannular patch for CHD presenting with gastroenteritis?

A

May have stiff RV = very dependent on preload for cardiac output to the lungs for oxygenation

172
Q

What are post-op complications of tetralogy of fallot? -do we worry if they get a URTI/LRTI?

A
  1. Severe PI –> dilated RV –> decreased RV function 2. Branch PA stenoses 3. Arrhythmias (RBBB) due to RV dilatation/transannular patch -since we expect them to be normal hemodynamically post-op, don’t worry about resp infections
173
Q

What is the surgical repair for TGA? -what are post-op complications? (3) -a patient post op TGA presents with chest pain. Worried or not worried?

A

Arterial switch operation at 2nd week of life (Jatene operation) -coronary buttons are reimplanted -LPA and RPA are draped in front of the aorta = pulling the PA anterior and can cause PA stenosis Post-op complications: 1. Branch PA stenosis 2. Proximal coronary button stenosis 3. Dilatation of ascending aorta Chest pain? = WORRY!

174
Q

Which CHD undergo norwood/glenn/fontan repair?

A

Overall: these have a single usuable ventricle and an unusable ventricle: No pulmonary output: TA, PA, PS, Ebstein’s OR No systemic output: HLHS, MS OR Unobstructed pulmonary flow: single ventricle with no PS, DORV with PS

175
Q

What is the Norwood 3 stage palliation? -ages for each?

A

Stage 1: norwood @ 7 d old Stage 2: Glenn @ 4-6 mo Stage 3: Fontan @ 3 yo

176
Q

What is the norwood operation? -what happens if you give these children O2?

A

Overall: want the heart to be one big bag that pumps to the body and not at all to the lungs 1. Atrial septectomy (take out the atrial septum completely) 2. Cut the MPA off the heart 3. Take the outflow tracts (aorta and MPA) and merge them with a patch (pericardium or gortex) = sew together = DKS = side to side anastamosis 4. BT shunt = systemic to pulmonary shunt = allows just enough blood to go to the PA from the systemic circulation -it does siphon away blood from the coronaries during diastole (blood can choose to go through the aorta to the coronary OR through the BTS to the PA…will usually choose BTS because pulmonary pressures are lower than systemic = this is why 30% of children die from this = coronary steal) -new procedure now = hybrid procedure: only put in a PDA stent with bilateral PA bands so that there is still pulmonary flow from the descending aorta without compromising coronary artery flow, then postpone the rest of the Atrial septectomy, MPA removal, etc. in Glenn procedure -normal stas: 75-85% -O2 causes pulmonary vasodilation and increases pulmonary blood flow; this is BAD because it STEALS the blood from their systemic circulation and can cause arrest so do NOT target 100% sats!

177
Q

What are the expected O2 sats for post-Glenn? -what happens if you give O2 to Glenn?

A

Normal sats = 75-85% -O2 causes pulmonary vasodilation and increases pulmonary blood flow and increase cardiac output since the blood will then go back to the body -if high PVR = blood can’t flow to lungs and thus blood can’t flow to the system since they have a SERIES circuit instead of parallel

178
Q

What are 3 questions to ask the patient who has gone through the Norwood 3 stage procedure? (ie. fontan is completed)

A
  1. What are your baseline sats? 2. Are you fenestrated? -protective mechanism against pulmonary hypertension -if the pressures in the lung are so high that blood can’t flow there, then at least the blood will flow from the extracardiac conduit (tube that connects IVC to PA) to the right atrium (that isn’t being used), through the ASD, into the LA –> LV to be pumped to the body = at least you’ll get some O2 to systemic circulation -this is why they are on anticoagulation = if they have a thrombus somewhere, can flow from right side to left side and get a stroke!!! Bad! -if yes: sats can be low 85% -if no, sats should be normal 3. Is your warfarin therapeutic?
179
Q

What is the Fontan procedure? -complications? (4)

A

Essentially, you cut the IVC off the heart and connect it to an extracardiac conduit which then connects to the PA -you do get sluggish flow 1. Fontan circuit obstruction (thrombosis, vascular stenosis) 2. Outflow obstruction 3. Ventricular dysfunction 4. Arrhythmias 5. Strokes

180
Q

What does 80% sat on a finger mean in a kid with a single ventricle?

A

Tells you there is equal bloodflow to the lungs and the body Ao sat% - SVC sat% / PV Sat % - PA sat% -Ao and PA sats should be the same -SVC sat % = expected to be 60% -PV sat% = expected to be 100% = 80-60/100-80 = 20/20 = 1:1 = this is why we target 80% sats! If sats = 90%, this tells you there is too much PBF and not enough to body If sats = 70%, there is too little PBF -if you have wet lungs, then this is BAD, means overcirculation BUT your sats will be high so don’t let this trick you

181
Q

What are the effects of the following on children with single ventricle pathophysiology? -URTI -Gastroenteritis Treatment?

A

Colds increase PVR thus decreasing PBF V&D decreases SBF from hypovolemia Treatment: GIVE VOLUME!!! Don’t be worried about giving them too much fluid!

182
Q

What is the cause of sinus arrhythmia?

A

Increased vagal tone -HR increases with inspiration, decreases with expiration

183
Q

What are 5 causes of first degree AV block?

A
  1. High vagal tone 2. Acute rheumatic fever 3. Hyper/hypokalemia, hypermagnesemia 4. Drug effect/toxicity (digoxin) 5. Lyme disease 6. CHD: ASD, AVSD, ebstein’s anomaly
184
Q

What are the 2 types of second degree AV block?

A

Mobitz I (Wenckebach): progressive PR lengthening prior to block -usually due to high vagal tone Mobitz II: no change in PR interval before block -THIS is the one that should worry us! 1. Exposure to maternal autoantibodies (ie. SLE) 2. Drugs 3. CHD

185
Q

How can you differentiate between 3rd degree AV block and JET?

A

Complete dissociation between the P waves and QRS complexes AND atrial rate > ventricular rate JET: complete dissociation between the P waves and QRS complexes but your ventricular rate > atrial rate

186
Q

What are 2 common causes of 3rd degree block?

A
  1. Postop CHD 2. Lyme disease
187
Q

What are PACs? -treatment?

A

Premature P waves differing in axis and morphology from normal sinus P waves -AV conduction may be normal, aberrant (BBB), or blocked -Rarely require treatment (50% newborns, 14-64% infants & children)

188
Q

How can you tell the difference between AVRT and AVNRT on ECG? (2)

A

AVRT = retrograde P waves following QRS, with RP interval > 0.07 sec -more common in infants/children AVNRT: retrograde P waves within QRS or at terminal end, RP internal < 0.07 sec -more common in teenagers

189
Q

How does the valsalva work for SVT?

A

Increases intra-thoracic pressure and affects baro-receptors (pressure sensors) within the arch of the aorta = increases vagal tone = needs to be in the supine position x 15 seconds

190
Q

What 5 medications can be used for acute treatment of SVT? -what 4 medications can be used for chronic treatment of SVT?

A

Acute treatment: 1. Adenosine 2. Verapamil 3. Procainamide 4. Esmolol 5. Amiodarone Chronic treatment: 1. Propranolol 2. Sotalol 3. Flecainide 4. Propafenone

191
Q

What 2 populations will you see atrial flutter in?

A

Atrial rates 250-480 bpm 1. Neonate with structurally normal heart 2. Older patient s/p CHD surgery

192
Q

What 2 populations will you see atrial fibrillation in? -treatment?

A

Atrial rates > 350 bpm “Irregularly irregular” ventricular response 1. CHD 2. Thyrotoxicosis -if no prior CHADS (congestive heart failure, hypertension, diabetes, stroke), no oral anticoagulation needed. Just cardiovert

193
Q

Why do we not worry about accelerated idioventricular tachycardia?

A

Not worrisome because starts and stops by itself, rate is not that much faster than sinus -still important to make sure heart is structurally normal with an ECHO

194
Q

How much deoxygenated hemoglobin must be present before you can clinically see cyanosis? -how does this change in a patient with anemia? -how does this change in a patient with polycythemia?

A

5 g/100 ml of deoxygenated hemoglobin must be present before cyanosis can be appreciated -in anemic patient: have much less hemoglobin so need higher percentage of reduced hemoglobin before cyanosis will be appreciated. Thus they might be hypoxemic without showing any cyanosis -in polycythemic patient: have much more hemoglobin so need lower percentage of reduced hemoglobin before cyanosis will be appreciated. Thus they might be cyanotic without actually being hypoxemic

195
Q

What is the treatment for hypertrophic cardiomyopathy?

A
  1. No competitive sports and strenuous physical activity = risk of sudden death 2. Beta blockers or calcium channel blockers = diminish ventricular outflow tract obstruction, modifies ventricular hypertrophy, improves ventricular filling 3. Anti arrhythmics or implantable cardioverter defibrillator = if patients have history of arrhythmias, strong family histories of arrhythmias or sudden death, patients with syncope 4. Screen first degree relatives with ECG and ECHO, genetic testing
196
Q

What are potential etiologies for torsades de pointes?

A

Think about anything that causes prolonged QT! Congenital: 1. Romano Ward 2. Jervell-Lange-Nielsen Acquired: 1. Electrolyte abnormalities: hypokalemia, hypomagnesemia, hypocalcemia 2. Medications: antipsychotics, antiarrhythmics, TCAs, antibiotics (macrolides) 3. Cardiac issues: myocarditis, post-op cardiac, etc. 4. Neurogenic: stroke, encephalitis, head trauma

197
Q

Which medication is CONTRAINDICATED in torsades de pointes?

A

Amiodarone!!! Can prolong QT further and worsen Torsades

198
Q

What is the treatment for Torsades De Pointes?

A

Magnesium 25-50 mg/kg x 1, followed by infusion upon discussion with Cardiology

199
Q

What is the management of pericarditis? (2)

A
  1. ASA/indomethacin/NSAIDs 2. Colchicine
200
Q

IE What are the clinical signs in iE?

A

1. General: unremitting fevers, fatigue, weight loss, and malaise

  1. Emboli from the vegetation:
    a. Emboli in a major artery (e.g., stroke, renal infarct, splenic infarct) if the vegetation is on the mitral or aortic valves
    b. Pulmonary embolism if the vegetation is on the tricuspid or pulmonic valves
    c. Mycotic aneurysm (or infected aneurysm or microbial arteritis)
    d. Intracranial and Conjunctival hemorrhages
    e. Janeway lesions: microabscesses of the dermis, appearing as nontender, erythematous macules or nodules on the palms and soles
  2. Immune complex deposition:
    a. Glomerulonephritis
    b. Osler nodes: painful, erythematous, raised lesions on the palms and soles
    c. Roth spots: retinal hemorrhages with pale centers
    d. Positive rheumatoid factor
201
Q

IE How do you Dx IE?

A

Infective endocarditis is diagnosed using the Modified Duke Criteria

  1. Blood cultures (at least two cultures from different sites) should be drawn for patients with fever of unexplained origin, a pathologic heart murmur, a history of heart disease, or previous endocarditis
  2. Echocardiography has a sensitivity of >80% when the diagnosis is suspected, but it cannot be used to rule out the diagnosis. Transesophageal echocardiography is more sensitive than transthoracic imaging. However, persistently positive blood cultures are the gold standard for diagnosis!
202
Q

IE What is the Duke Criteria - Clinical for Dx of IE?

A

2 major clinical criteria
OR
1 major and 3 minor clinical criteria
OR
5 minor clinical criteria

203
Q

IE What are the MAJOR Duke Criteria?

A
  1. Positive blood culture for infective endocarditis

Typical microorganisms consistent with infective endocarditis from 2 separate blood cultures
OR
Persistently positive blood culture
OR
Single positive blood culture for Coxiella burnetii or phase I IgG antibody titer >1:800

  1. Evidence of endocardial involvement:
    a. Positive echo

Vegetation
OR
Abscess
OR
New partial dehiscence of a prosthetic valve

b. New valvular regurgitation on echo

204
Q

IE What are the 5 MINOR Duke Criteria?

A
  1. Predisposing factor: IV drug use or presence of a predisposing cardiac condition
  2. Fever ≥38.0°C
  3. Phenomena- Vascular OR Immunologic
  4. Microbiologic evidence: positive blood cultures that do not meet major criteria, or active infection with an organism consistent with infective endocarditis
205
Q

IE What are the 2007 US recommendations for prophylaxis for iE?

A

Intro:

a. Anatomy: For dental procedures and perforation of the oral mucosa, No longer recommended for patients undergoing GIT or GUT procedures
b. Patient risk; In general, prophylaxis is recommended only for high-risk patients (not moderate risk)

Guidelines;

  1. Prosthetic cardiac valve or prosthetic material used for repair of a valve
  2. Previous infective endocarditis
  3. Congenital heart disease:
    a. Unrepaired cyanotic CHD, including palliative shunts and conduits
    b. Completely repaired CHD with prosthetic material or device (placed surgically or by catheter) for the FIRST 6 months after the procedure

C. Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (that could inhibit endothelialization)

  1. Cardiac transplant recipients with cardiac valvulopathy
206
Q
A
207
Q

IE What is the advice for IE Prophylaxis for MVP?

A
  • MVP is the most common underlying condition that predisposes to the acquisition of IE in the western world, but the absolute incidence of IE is extremely low in this population.
  • In addition, IE with MVP is not usually associated with the grave outcomes associated with the conditions noted above.
  • Consequently, IE prophylaxis is no longer recommended for patients with MVP.
208
Q

IE Which dental procedures do NOT need IE Prophylaxis?

A
  • Routine anesthetic injections through noninfected tissue, taking dental radiographs,
  • placement of removable prosthodontic or orthodontic appliances,
  • adjustment of orthodontic appliances,
  • placement of orthodontic brackets,
  • shedding of deciduous teeth
  • bleeding from trauma to the lips or oral mucosa.
209
Q

IE What is the Antibiotic regimen to prevent IE for dental and other procedures?

A
  • Antibiotics for prophylaxis should be administered in a single dose before the procedure.
  • If the antibiotic is inadvertently not given before the procedure, it may be administered up to 2 h after the procedure.
  • It should be noted that rarely, some patients who are scheduled for an invasive procedure may have a coincidental IE. The presence of fever or other manifestations of systemic infection should alert the provider to the possibility of IE, and it is important to obtain blood cultures and other relevant tests before administration of antibiotics intended to prevent IE.
210
Q

IE Which specific antibiotics are recommended for IE prevention?

A
  1. Amoxicillin -well absorbed +high and serum concentrations. 2. Allergic to penicillin or amoxicillin (no anaphylaxis) cephalexin, clindamycin, azithromycin or clarithromycin
  2. If systemic anaphylaxis DO not use cephalosporin
  3. Unable to tolerate an oral antibiotic may be treated with parenteral ampicillin, ceftriaxone or cefazolin.
  4. Ampicillin-allergic patients who are unable to tolerate an oral agent may be treated with parenteral _cefazolin, ceftriaxone or clindamycin (_avoiding the cephalosporins if there is a history of anaphylaxis, angioedema or urticaria).
211
Q

Syncope How do neurogenic and cardiac syncope compare?

A
212
Q

QTS How do you measure it?

A
213
Q

WPW What is it?

A

Accessory atrioventricular pathway allows “early”

depolarization of ventricles (pre-excitation)

214
Q

WPW What conditions is it associated with?

What are the ECG features?

A

Associated with Ebsteins and CCTGA

ECG features?

• Seen only in sinus rhythm:

– Short PR interval

– delta wave

215
Q

WPW What rhythyms can it cause?

A
  1. SVT - retrograde conduction through accessory pathway
  2. Sudden death - rapid antegrade conduction of atrial

arrhythmia

216
Q

WPW treatment?

A

Optimal treatment controversial

  1. No symptoms – No treatment
  2. SVT – beta blockers or ablation (no digoxin)
  3. Fainting with palpitations - ablation
217
Q

RSV and CHD What are the RSV and otehr vaccine recommendations?

A

Palivizumab™ = Monoclonal IgG antibody against RSV

CPS - RSV vaccine if < 1 year old

  1. with cyanotic CHD or
  2. hemodynamically significant acyanotic CHD (requiring meds)

– Given in 5 doses beginning with start of season

– Give anytime after OR

N.B.

a. Flu shot also recommended for those over 6mo
b. Regular immunizations given on schedule

218
Q

RSV vaccine update CPS?

A

The administration of palivizumab, which is given once monthly by injection, is no longer routinely recommended for babies born after 30 weeks unless they have chronic lung disease or congenital heart disease.

219
Q
A
220
Q

IE What do the following lesions look like?

Janeway, splinter hemorrhage, emboli, osler nodes

A

PEDIATRICS EXAM REVISION (56 decks)

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