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Pediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the underlying pathology of PDA?

A

PDA - connection between the Aorta and the Pulmonary artery

Once pulmonary resistance falls, blood flows L to R into the pulmonary artery which can result in over-circulation into the lungs, wide pulse pressure and pulmonary vascular disease (like a VSD)

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2
Q

What causes normal physiological splitting of the S2?

A

Delayed closure of the PV with respect to AV (usually as a result of deep inspiration)

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3
Q

How do the heart sounds change in the setting of PPHN?

A

Fixed single S2 (increased PVR will prevent any obvious splitting of S2)

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4
Q

What dose of prostaglandin should be used in treatment of suspected congenital heart disease?

A

0.01 - 0.02 µg/kg/min

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5
Q

What are the short and long term side effects of prostaglandin?

A 
Short term:
• Apnea
• Skin flushing
• Fever
• Seizure-like activity
• Hypotension
• Bradycardia
Long term:
• Periosteal hyperostosis
• Gastric outlet obstruction
• Necrotizing enterocolitis
• Diarrhea
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6
Q

Where do the majority of coarctations take place?

A

Just below (after) the origin of the L subclavian artery (98%)

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7
Q

How does prostaglandin help palliate the changes caused by coarctation of the aorta?

A

Prostaglandins help maintain the patency of the PDA, which in turn, may serve to widen the juxtaductal area of the aorta and provide temporary relief from the obstruction

As such, perfusion to the lower half of the body becomes dependent on the PDA and consequently, the RV output

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8
Q

What is the mechanism for radial-femoral delay?

A

Given the presence of coarctation, blood flow to the lower half of the body is reliant on collateral vessels. Otherwise, normally the femoral pulse should be felt before the radial pulses

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9
Q

What difference is acceptable with respect to BP measured in the upper and lower extremities?

A

Legs should be 10-20 mmHg higher than that of the upper extremities

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10
Q

What bony changes can be caused by a severe coarctation?

A

Notching of the inferior border of the ribs

pressure erosion by enlarged collateral vessels; common by late childhood

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11
Q

Once a coarctation is discovered, when should repair take place?

A

Once the patient has been stabilized; age and growth are not reasons for delaying surgical repair of coarctation

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12
Q

A child has just had their coarctation repaired when they develop rebound hypertension and abdominal pain. What is the mechanism?

A

Postcoarctectomy Syndrome

Postoperative mesenteric arteritis may be associated with acute hypertension and abdominal pain in the immediate postoperative period

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13
Q

What is the treatment of choice in a young child who has had re-coarctation despite a successful coarctectomy?

A

Balloon angioplasty

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14
Q

What congenital heart defect can lead to ST changes in the anterolateral leads (avL, V5, V6)?

A

ALCAPA
• Anomalous left coronary arteries from pulmonary artery
• Presents in teens/young adulthood unless there are no collaterals

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15
Q

What congenital heart defects are seen/associated with R aortic arch?

A
  • Tetrology of Fallot
  • Truncus arteriosus

Otherwise, patients tend to be asymptomatic

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16
Q

What conditions are associated with vascular ring?

A

Anomalous L sided vessels (PA, innominate and carotid arteries), double aortic arch, or R aortic arch with L ligamentum arteriosum

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17
Q

What cardiac lesions are linked to the following genetic conditions?

Down Syndrome
DiGeorge Syndrome
Williams Syndrome
Turner Syndrome
Marfan Syndrome
A 
Down syndrome – AVSD
DiGeorge – TOF
Williams – supravalvular aortic stenosis
Turner – coarct, bicuspid AoV
Marfan - dilated aortic root, MVP
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18
Q

What are some indications for treatment of PVCs?

A
  • 2+ PVCs in a row
  • Multiform PVCs
  • Increased PVCs with activity (should decrease)
  • R-on-T phenomenon (PVC depolarization on T-wave of preceding beat)
  • Extreme frequency (>20% total beats on Holter)
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19
Q

What is the most common cause of SVT in infants?

A

Atrioventricular reciprocating tachycardia (AVRT) as the result of an accessory pathway

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20
Q

What are the 4 major categories of SVT?

A
  1. Reentrant tachycardias using an accessory pathway
    - AVRT - Most common mechanism of SVT in infants
  2. Reentrant tachycardias without an accessory pathway
    - Atrioventricular node reentry tachycardia (AVNRT); increasing incidence in childhood and into adolescence, associated with exercise, 2 pathways (fast and slow)
  3. Ectopic or automatic tachycardias
    - Common in patients following cardiac surgery or with cardiomyopathy
  4. Chaotic/multifocal atrial tachycardia
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21
Q

What is the most ominous sign in a patient with SVT?

A

Syncope with WPW Syndrome; these patients need catheter ablation

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22
Q

What treatment options are available for children with acute runs of SVT?

A

• Abortion maneuvers (vagal stimulation with ice, Valsalva maneuver, straining, breath holding, or standing on their head)
○ Ocular pressure must never be performed, and carotid sinus massage is very rarely effective

• Pharmacologic alternatives
○ Adenosine by rapid IV push (tx of choice); Never give without a means for DC cardioversion
○ CCB (i.e. verapamil) in older children (contraindicated if <1 year)
○ Procanimide
○ Amiodarone

• Synchronized DC cardioversion (0.5-2 J/kg) is recommended as the initial management in unstable patients

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23
Q

What medication should be used in the case of children with WPW?

A

→ β-blockers

digoxin or CCB may increase the rate of antegrade conduction of impulses through the bypass tract, with the possibility of ventricular fibrillation, and are therefore contraindicated

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24
Q

What is the most common cardiac malformation?

A

VSD (25%) (14-18% based on HSC lecture)

25
Q

What is Ebstein’s anomaly?

A

Abnormal displacement of tricuspid valve into the RV creating a thin-walled larger atria and a smaller RV. If RV is unable to generate adequate force to push blood out of the PV, functional pulmonic atresia

26
Q

What findings would you expect on CXR and ECG for a patient with Ebstein’s anomaly?

A
  • Enlarged heart (RA)
  • RBBB (pt are at risk of arrhythmias), prolonged PR, delta waves
  • Holosystolic murmur as a result of Tricuspid regurgitation
27
Q

What is the mechanism behind protein losing enteropathy in children who has recently undergone Fontan?

A

Secondary to chronically low CO which results in poor perfusion of gastrointestinal mucosa along with reduced mesenteric vascular impedance and congestion

  • Passive blood flow into the lungs results in elevated venous pressures; in turn, causes abnormal enterocyte function
28
Q

What treatment should be considered in cases of post-Fontan protein losing enteropathy?

A
  • Oral budesonide (reduces protein loss)
  • Sildenafil (to reduce pulmonary artery resistance)
  • Dietary changes: minimize anemia, augment calories (high protein, high MCTs, low sodium, low fat is recommended)
  • Diuretics to treat symptoms of volume overload
  • Cardiac transplantation post-Fontan
29
Q

What are the 3 types of heart block?

A
  • First degree heart block - PR interval >200 ms
  • Second degree heart block
    • Mobitz Type 1 - Wenckebach - gradual prolongation of PR interval until one beat is dropped
    • Mobitz Type 2 - consistently long PR interval with one beat being dropped
  • Third degree heart block- complete heart block - complete disassociation of atria and ventricles
30
Q

What is the most common innocent murmur of childhood?

A

Still’s Murmur

  • Infancy to adolescence; most common between 3 and 6 years
  • Usually Grade 1-3, low-frequency murmur heard best over the LLSB as well as the cardiac apex
  • Vibratory or musical quality that has been likened to the vibrations of a taut string; loudest when the child is in the supine position
  • Varies with respiration; louder in expiration and becomes softer with deep inspiration
  • Increased velocity of flow as blood is pumped into the aorta from the LV, or vibrations of the MV chordae or LV false tendons
  • Warrants no additional investigation
31
Q

What is the only benign murmur that is best heard in the upright position?

A

Venous Hum

Pulmonary flow murmur of childhood and Still’s murmur are both better heard in supine position

32
Q

What are the most common bacterial agents in cases of infective endocarditis?

A

Strep viridans and Staph aureus

Central venous catether - CoNS
(IVDU - pseudomonas, serratia)

33
Q

What are Duke’s Criteria?

A

Duke Criteria (2 major OR 1 major 3 minor OR 5 minor)

  • Major: BCx (2 separate, usual pathogens OR 2+ for less typical), evidence of endocarditis on echo (intracardiac mass on valve or other, regurgitant flow near prosthesis, abscess, partial dehiscence prosthetic valve, new valve regurg)
  • Minor: predisposing condition, fever, embolic-vascular signs, immune complex (GN, arthritis, RF, osler nodes, roth spots), single BCx+ or serologic evidence infection, echo signs (NOT meeting major criteria)
34
Q

6 indications for endocarditis prophylaxis?

A
  • Prosthetic cardiac valves
  • Previous infective endocarditis
  • Unrepaired cyanotic congenital heart disease, including palliative shunts and conduits
  • Completely repaired congenital heart defect with prosthetic material or device, during the first 6 months after the procedure
  • Repaired congenital heart disease with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (inhibits endothelialization)
  • Cardiac transplant recipients with cardiac valvulopathy
35
Q

What are 4 reasons the infective endocarditis guidelines were modified?

A
  • IE is much more likely to result from frequent exposure to random bacteremias associated with daily activities than from bacteremia caused by a dental, GI tract or GU tract procedure
  • Prophylaxis prevents an exceedingly small number of cases of IE
  • The risk of antibiotic-associated adverse events exceeds the benefit, except in very high-risk situations
  • Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia from daily activities, and is more important than the use of prophylactic antibiotics for dental procedures
36
Q

What treatment can be offered a child with truncus arteriosus?

A
  • Initially, medications to aid with pulmonary congestion i.e. diuretics
  • Surgery to redirect blood flow and prevent pulmonary congestion via conduits (will need repeated replacements overtime as they are prone to congestion and regurgitation)
37
Q

What are the 4 features of Tetrology of Fallot?

A
  • Over-riding, R-sided aorta
  • VSD
  • RV outflow obstruction
  • RVH
38
Q

What measures can be taken in the event of a “tet spell”?

A
  • Calm the child i.e. have parent comfort
  • Oxygen
  • Morphine (max 0.2 mg/kg), ketamine
  • Position in knee-chest position
  • Sodium bicarb if tet spell is prolonged or severe to treat acidosis
  • Increase SVR (phenylepherine, norepi)
  • Propranolol to stop infundibular spasm
39
Q

What is required for a child to TAPVR to survive?

A

ASD

otherwise: Systemic circulation → RA → RV → PA → lungs → RA

40
Q

Which of the TORCH infections is associated with PDA?

A

Maternal rubella infection in early pregnancy

41
Q

Potential causes of dilated cardiomyopathy?

A

Idiopathic, Duchenne’s Muscular Dystrophy and Becker’s Muscular Dystrophy, mitochondrial myopathies, FAO defects, nutritional deficiencies, severe anemia, doxorubicin

42
Q

What ECG changes will you see in the case of hypertrophic cardiomyopathy? What genetic conditions are associated with this?

A

Prominent P waves, a short P-R interval, and massive QRS voltages

Pompe Disease and Noonan Syndrome

43
Q

What are the pathological differences between dilated and hypertrophic cardiomyopathy

A

Dilated - ventricular failure, poor CO, arrhythmias

Hypertrophic - restrictive pattern with impaired filling, diminished compliance and subsequent poor CO

44
Q

What are 3 antibiotic classes that can prolong QT?

A
  • Sulfonamides - Septra
  • Macrolides - Erythromycin
  • Fluoroquinolones - Ciprofloxacin
45
Q

What are the genotypic-phenotypic correlations seen in LQTS?

A

EAR
1 - exercise/swimming
2 - auditory
3 - rest/sleep

46
Q

What is the first line treatment for prolonged QT syndrome?

A

Beta blockers

47
Q

What is the criteria for normal sinus rhythm?

A
  • P wave before every QRS complex
  • QRS complex after every P wave
  • Normal P wave morphology
48
Q

How do you determine the heart rate on an ECG

A
  • 300, 150, 100, 75, 50 rule

* number of QRS complexes on the rhythm strip x 6

49
Q

What are potential causes for superior axis?

A
  • Noonan syndrome, left anterior fascicular block, some types of WPW
  • Pink and superior axis → AVSD
  • Blue and superior axis → tricuspid atresia
50
Q

What are the ECG features seen in cases of bundle branch block?

A

• Conduction delay in the bundle branches → specific abnormal QRS morphology
- “WillaM and MorroW”

  • Morphology + long QRS duration = complete bundle branch block
  • Morphology + normal QRS duration = incomplete
51
Q

What is Bazzett’s formula?

A

QTc = QT/square root of R-R

52
Q

What findings are noted on ECG in LVH? LV strain?

A

Left ventricular hypertrophy
• Tall R waves in V6 (V5); borderline deep S wave in V1 (V2)
• Left axis deviation for age

Left ventricular strain
• ST depression with T wave inversion in V6
• Compensatory ST elevation in V1, V2

53
Q

What ECG findings indicate RVH? RV strain?

A
  • Deep S waves in V6; Tall R waves in V1
  • Right axis deviation for age

Right ventricular strain pattern
• Upright T wave in V1 (from 1 week to 6 years)

54
Q

What findings on ECG would indicate LA hypertrophy?

A

Left atrial enlargement:
• Wide, notched P waves in any limb lead
• Large negative component of P wave in V1

55
Q

What are some examples of abnormal T-wave changes on ECG?

A

Flat or inverted:

  • Ventricular hypertrophy (with strain)
  • Inflammation (myocarditis, myopericarditis)
  • Ischemia (i.e. coronary abnormality)

Tall/peaked: hyperkalemia

Long: certain types of long QT syndrome, hypokalemia

56
Q

What conditions are associated with ST elevations?

A

Pericarditis, hypertrophy with strain, perfusion abnormality, arrhythmia, inflammation (myocarditis)

57
Q

What are the 5 most common forms of cyanotic heart disease?

A
  • Tetralogy of Fallot (10%)
  • Transposition of the great arteries
  • Truncus arteriosus
  • Total anomalous pulmonary venous return
  • Tricuspid valve abnormalities: Atresia, Ebstein’s
58
Q

How do you do a hyperoxia test?

A

Apply 100% O2 and test the arterial response

With intracardiac right to left shunt the p02 does not exceed 100 mm Hg and the rise is usually not more than 10 to 30 mm Hg in an arterial blood gas

59
Q

What maternal conditions may cause CHD?

A

Diabetes mellitus: TGA, VSD, HCM
Lupus erythematodes: AV block III
Lithium: Ebstein’s anomaly
Hydantoin: AS, PS

Pediatrics (27 decks)

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