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Pediatric Board > cardiology > Flashcards

cardiology Flashcards

1
Q

What is seen in peripheral cyanosis vs. central cyanosis?

A

peripheral: normal oxygen saturation but less circulation to periphery due to cold, polycythemia
blue extremities but trunk, mucous membranes are pink
central: due to arterial desaturation, blue lips, mucus membranes, and trunk

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2
Q

What is differential cyanosis and what does it mean?

A

cyanosis of lower extremities / toes but no the fingers or upper extremities
aortic arch obstruction
persistent pulmonary hypertension

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3
Q

What is reverse differential cyanosis?

A

cyanosis of pre-ductal structures : fingers but not post ductal structures (toes)
transposition of the great vessels with right to left shunting of saturated blood

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4
Q

What does significant delay or absence of the femoral pulse compared to the radial pulse indicate

A

coarctation of the aorta

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5
Q

What does rapid rising or bounding pulses indicate

A

PDA

aortic valve insufficiency

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6
Q

When do you hear ejection clicks and what can it indicate

A

beginning of S1
thickened semilunar valve (bicuspid aortic valve, aortic stenosis pulmonic stenosis)
truncus arteriosus
enlarged aorta (tetralogy of fallot)

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7
Q

What is the difference between aortic stenosis and pulmonic stenosis on exam

A

pulmonic stenosis ejection click varies with inspiration

aortic stenosis ejection click does not

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8
Q

What does wide persistent fixed splitting of S2 indicate

A

ASD, pulmonic stenosis, RBBB

delayed right ventricular emptying

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9
Q

What are the characteristics of an innocent murmur

A

short and soft grade III/IV
louder supine
soft or disappear with valsalva

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10
Q

Describe a still’s murmur

A

systolic ejection murmur with a musical quality or vibratory character
hear best in the precordial area but not in the back

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11
Q

What is physiologic peripheral pulmonic stenosis

A

right and left pulmonary arteries are smaller than main pulmonary artery
harsh ejection murmur heard in the axilla and both right and left hemi-thoraces
improves by 12 months of age

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12
Q

Describe a venous hum

A

blood draining down the collapsed jugular veins
absent when supine
Valsalva, turning of the head, or compression of the jugular vein makes the murmur go away

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13
Q

How does the axis deviation change from birth to childhood

A

right ventricular dominance at birth results in right axis deviation (70-180) and large R wave in V1 at birth
in an older child > 100 is RAD, < -30 is LAD

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14
Q

What is a quick way to determine the axis?

A

if I and AVF are both + = normal
if I + and AVF - = look for LAD
if both are - = extreme axis deviation
if I - and AVF + = look for RAD

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15
Q

what is the rate of each mm on EKG tracing

A

0.04 ms

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16
Q

What is Dubin’s way to calculate the rate

A

number of large boxes between R-R

300, 150, 100, 75, 60, 50

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17
Q

What is a normal PR interval

A

3-5 small boxes or 120 to 200 ms

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18
Q

What is a normal QRS duration

A

< 120 ms or 3 small boxes

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19
Q

What is a normal QTc

A

< 450 usually 340 to 440

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20
Q

How do you calculate the QTc

A

QT / (RR) ^ 1/2

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21
Q

What is the problem with a prolonged QT

A

tendency to develop sudden death, syncope due to polymorphic VT or torsades

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22
Q

What are two syndromes to consider in a child who has a long QT and sensoriuneural deafness

A

Jervell

Lange-Nielsen syndrome

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23
Q

What are some causes of QT prolongation

A 
TCA overdose
hypocalcemia
hypokalemia
hypomagnesemia
CNS insult
starvation with electrolyte abnormalities
Type 1a and type3 antiarrhythmics
azithromycin
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24
Q

What does a normal p wave look like

A

3 small square in duration
2 mm in height
normal are up in I, II, AVF and down in AVR

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25
Q

What is seen on EKG in brugada syndrome

A

RV conduction delay and ST elevation in V1-V3

sodium chanelopathy

26
Q

What is a sign of R atrial enlargement

A

normal width, increased amplitude

27
Q

What is a sign of L atrial enlargement

A

wide p wave taking up most of the PR interval

m shaped p wave

28
Q

What direction should the t wave be in V1

A

after birth for the first week, t wave is positive in V1,
after that it should be inverted
if it is not indicates RVH

29
Q

What can cause peaked T waves

A

hyperkalemia

intracerebral hemorrhage

30
Q

What causes ST segment elevation

A

MI, prinzmetal angina

pericarditis-most common, will be diffuse st elevation

31
Q

What causes ST segment depression

A 
subendocardial ischemia
LHV with strain
digitalis
hypokalemia
RVH
32
Q

How is LVH diagnosed on an EKG

A

left axis deviation
voltage criteria: r wave less than the 5th percentile, S wave > 95% in V3R and V1 or R waves more than 95th % in V5 and V6

33
Q

What are ways to diagnose RVH on EKG

A

upright or flat T wave in V1, in child < 1 week to 8 years of age
R > 25 mm in right chest leads

34
Q

What is 1 degree AV block

A

PR interval > 200 ms (5 small boxes) or more than normal for age

35
Q

What is 2 degree AV block Mobitz type 1

A

wenchebach progressive prolongation of the PR interval until the QRS drops

36
Q

What is 2 degree AV block Mobitz type 2

A

normal PR interval with periodic drop of QRS

often requires a pacemaker

37
Q

What is 3rd degree AV block

A

complete AV dissociation
often needs pacemaker
if rate is 40-60 with a normal QRS width likely a junctional escape rhythm
if rate is 20-40 and QRS is wide, likely a ventricular escape rhythm

38
Q

What are some mechanisms that cause SVT

A 
atrioventricular re-entry (accessory bypass tract): leading cause in children of SVT
AV nodal re-entry
automatic rhythms (accelerated atopic rhythms)
39
Q

What are the indications for pacemaker in children with sick sinus syndrome

A

patient is symptomatic

patient has tachyarrhythmia that requires therapy and therapy might precipitate significant bradycardia

40
Q

How might sick sinus syndrome present

A

abnormal sinus bradycardia, sinus pauses, sinus arrest, tachy-brady syndrome
esp in child who has had atrial surgery (ASD repair, fontan, transposition correction)

41
Q

How should atrial flutter be managed

A

most effective treatment is synchronized cardioversion
vagal maneuvers slow rate for diagnosis
rule out PE, and thyroid disease if no prior cardiac history
can control rate with diltiazem, digoxin or a beta blocker
ablation is a definitive treatment

42
Q

How should atrial fibrillation be managed

A

irregular ventricular rate 130-200
if new consider hyperthyroidism, hypomagnesemia, alcoholism/cocaine abuse and excessive caffeine and nicotine
anticoagulated 3 weeks prior to and 6 months after cardioversion
can again use beta blockers, diltiazem and digoxin for rate control

43
Q

How is paroxysmal SVT treated

A

vagal maneuvers (ice), adenosine
no verapamil in those < 1 year
if unstable -> cardioversion

44
Q

What is WPW

A

shortened PR interval and a delta wave prior to QRS since there a bypass bundle (kent bundle) that depolarizes faster than the AV node

45
Q

How do you treat WPW and a narrow complex tachycardia? What do you not do?

A

Same as SVT. Vagal maneuvers, adenosine
Never: treat WPW in atrial fib or flutter with digoxin, verapamil or beta blockers
Instead: IV procainamide
shock if unstable
ablation is the definitive treatment of choice

46
Q

What is the treatment for PVCs

A

if there are symptomatic: nothing

if paired and no underlying heart disease: no not treat

47
Q

What do you do with ventricular tachycardia

A

if unstable: cardioversion
if stable: amiodarone
there is a benign form with child with a slow ventricular rhythm at the same rate or slightly faster than a sinus rhythm this does not need treatment and child is asymptomatic: if usually resolves with time

48
Q

Causes of ventricular tachycardia

A 
electrolyte disturbances
myocardial disease (myocarditis or hypertrophic cardiomyopathy)
ion channel disorders (Long QT)
postoperative states
ingestion
hypoxia
idiopathic
49
Q

When to avoid verapamil

A 
in children < 1 year
atrial fibrillation in WPW
atrial flutter
wide complex tachycardias
with beta blockers
50
Q

What can be a side effect of adenosine

A

bronchoconstriction

treat with bronchodilator

51
Q

What are the side effects to class 1a antiarrhythmics Quinidine and procainamide

A

both prolong the QT -> torsades
Quinidine: diarrhea, ITP, cinchonism: hearing loss, tinnitus and psychosis
Procainamide: blood dyscrasias (neutropenia, thrombocytopenia) drug induced lupus, caution in heart failure

52
Q

What are the side effects to class 1b antiarrhythmics lidocaine

A

seizures

53
Q

What are the side effects to class II antiarrhythmics beta blockers

A

bradycardia and potential aggravation of asthma

54
Q

What are the side effects to class 3 antiarrhythmics bretylium and amiodarone

A

bretylium: transient hypertension that postural hypotension
amiodarone: corneal deposits, pulmonary fibrosis, gray skin, hyper/hypothyroidism, hepatic toxicity and sun sensitivity

55
Q

When does left to right shunting start to become most apparent in a child

A

weeks 4-8 when pulmonary vascular resistance falls

56
Q

What happens if left to right shunts are not corrected

A

persistent elevated pulmonary pressures results in fixed pulmonary vascular resistance (pulmonary hypertension) and subsequent right to left shunting -> lethal)

57
Q

What are the main left to right shunting lesions

A 
PDA
ASD
VSD
AV canal defect
L transposition of the great arteries 
sinus of Valsalva fistula
58
Q

How does a PDA present

A

continuous murmur
rumbling, machine like
wide pulse pressure, bounding pulse
PDA is often closed surgically even in those who are asymptomatic

59
Q

What type of VSDs are most common in which age group

A

in those less than 1 year: usually muscular septum and most close spontaneously
in those > 1 year: membranous septum and do not close spontaneously

60
Q

How is a VSD diagnosed

A

harsh murmur at the lower left sternal border

if large, CXR with cardiac enlargement and pulmonary vascular markings

Pediatric Board (11 decks)

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