Transcript Pediatric Cardiology

Pediatric
Cardiology
Cyanosis
Definition,
Visible cyanosis,
Types:
1-peripheral(acrocyanosis) --->
definition….
causes:
A:hypetermia
B:low cardiac output
2-central--->definition…
causes :
A: Methemoglobinemia
B:Disorders of O2 penetration into circulatory
system
C:Rt to Lt shunt at cardiac or pulmonic level
Clubbing
Congenital cardiac disease causes of finger
clubbing
Finger clubbing can also be caused by congenital
cardiac diseases including:
Tetralogy of Fallot (combination of four structural
defects)
Total anomalous pulmonary venous return (TAPVR;
rare condition in which the pulmonary veins do not
empty into the heart)
Transposition of the great vessels (rare condition in
which the major vessels entering or leaving the
heart are misconnected
Respiratory disease causes of finger clubbing
Finger clubbing may be caused by respiratory diseases
including:
Bronchiectasis (destruction and widening of the large
airways)
Chronic obstructive pulmonary disease (COPD),
including emphysema and chronic bronchitis
Cystic fibrosis (thick mucus in the lungs and respiratory
tract)
Lung abscess
Lung cancer
Pulmonary fibrosis (scarring of the lungs)
s
Gastrointestinal disease causes of finger clubbing
Finger clubbing can also be caused by gastrointestinal
diseases including:
Celiac disease (severe sensitivity to gluten from wheat
and other grains that causes intestinal damage)
Cirrhosis of the liver
Inflammatory bowel disease (includes Crohn’s disease
and ulcerative colitis)
Liver cancer.
Other causes of finger clubbing
Finger clubbing can also have other causes including:
Dysentery (infectious inflammation of the colon, causin
severe diarrhea)
Graves’ disease (type of hyperthyroidism resulting in
excessive thyroid hormone production)
Hodgkin’s lymphoma (cancer of the lymph tissues)
Cardiac murmurs
1-Innocent :
A:Still’s murmur---> the most common
B:Pulmonic flow murmur of infancy
C:Pulmonic flow murmur of childhood
D:Venous hum
2-Pathologic murmurs:
A:Ejection systolic
B:Holosystolic
C:Diastolic
D:Continious
E:To & fro
F:Tumor plop
Chest pain
A:Non cardiogenic
Non specific chest pain is the most common
cause
1-Costochondritis
2-Tietze syndrome
3-Precordial catch syndrome
4-slipping rib syndrome
5-Hyper sensetive xyphoid
6-Trauma & muscle strain
7-Sickle crisis
8-Herpes zoster ,pneumonia,bronchitis
9-GE reflux
10-Pneumothorax
B:Cardiogenic
1-AS
2-Obstructive HCM
3-Pericarditis
4-Aortic dissection….Marfan syndrome
5-MVP
6-Arrhythmia
7-Abnormality of coronary arteries--->Kawasaki
a: Abnormal origin of CAs---->ALCAPA ,ARCAPA
b: Abnormal course of CAs--->Intramural,
Intramuscular,
Interarterial
c: Coronary cameral fistula
Palpitation
Ask the patient for mimic heart sound or rhythm Pounding
heart ,
Abrupt beat , Pause
Paroxismal or slowly onset & ending
Relationship with :Anxity / Emotion, Exercise
Duration (transient or incessent)
Coming with: Angina,
Syncopy/Presyncopy ,
Significant breath stopping
Causes:
Non cardiogenic:
1-Anxity,pain,fare,fevere,anemia,hypovolemiah
2-Hyperthyroidism,Pheochromocytoma,
neuroblastoma, carcinoid syndrome
3-GE reflux
Cardiogenic:
1-Arrhythmia
2-LV disfunction
Evaluation:
Hb/Hct , Urea, Potasium, Ca ,Mg
TFT
12 leads ECG
Echocardiography
24-H ECG Holter monitoring
Patient activated ECG recorder
Implantable loop recorder
Congenital
Heart
Disease
1-Acyanotic:
A:Normal pulmonic flow
B:High pulmonic flow
2-Cyanotic:
A:Low pulmonic flow
B:High pulmonic flow
Acyanotic Nl pulmonic flow disease:
All type of obstructive or regurgitant inflow or
outflow tracts.
Acyanotic high pulmonic flow disease:
ASD ,Gerbod’s defect ,VSD ,PDA ,
Aorto-pulmonary window ,PAPVC
Atrial Septal
Defect
Septal defects:
Inter atrial communication :
Secundum ASD(the most common type)
Primum ASD(is associated with MV cleft)
Sinus venosous defect (SVC type ASD)
Coronary sinus defect
IVC type ASD
Common atrium
According to Fossa Ovalis:
PFO or ASD2
ASD1(Ant)
Sinus venosous defect(Ant &Sup)
Coronary sinus defect(Ant &Inf)
IVC type ASD (Post & Inf )
Common atrium (near or total absence of inter
atrial septum)
Anatomic closure of foramen oval in the first
year of life.
No closure: 25-30%
PFO : < or = 3.5mm
Small ASD2 : 3.5-5mm
Mod : 5-8mm
Large : > 8mm
Overally the clinical manifestations
of ASDs depend on magnitude of
intracardiac shunt.
Most infants with ASDs are asymptomatic, and
the condition goes undetected. They may
present at 6 to 8 weeks of age with a soft
systolic ejection murmur and possibly a fixed
and widely split S2.
Older children with a moderate left-to-right
shunt often are asymptomatic.
Children with large left-to-right shunts are likely
to complain of some fatigue and dyspnea.
Growth failure is very uncommon.
Rarely, ASDs in infants are associated with
poor growth,
recurrent lower respiratory tract infection,
and heart failure.
Kalifornia- Fire waterfall
Congestive heart failure rarely is found in the first
decades of life, but it can become common once
the patient is older than 40 years of age .
The onset of atrial fibrillation or, less commonly,
atrial flutter can be a hallmark in the course of
patients with ASDs.
The incidence of atrial arrhythmias increases with
advancing age to as high as 13% in patients older
than 40 years of age and 52% in those older than
60 years of age .
Pulmonary vascular disease can occur in 5% to
10% of patients with untreated ASDs,
predominantly in females .
Usually it occurs after 20 years of age, although
rare cases in early childhood have been
recorded .
ECG:
RAD , RAE
rsR’ in V1 (in complet RBBB)
Outcome:
Secundum ASDs can close spontaneously,
remain open, or enlarge.
It appears that spontaneous closure, or a
decrease in size, is most likely to occur
in ASDs <7 to 8 mm and with younger age at
diagnosis.
Spontaneous closure occures in all ASDs <3 mm in
diameter, 87% of 3 to 5 mm , 80% of 5- to 8-mm
ASDs, and in none of infants with defects >8 mm.
No follow-up is necessary if a defect is <3 mm in
diameter, but for those with a defect 3 to 5 mm
or 5 to 8 mm, they should be evaluated by the
end of the 12th and 15th month, respectively, by
which time >80% of the defects will be closed.
In significant secundum ASDs at follow up 22%
are closed spontaneously before 1year old,
33% between 1 and 2 years old and
3% between 2 and 4 years.
Thus overally recommendation is to wait until
after age 4 years for elective closure.
Since most ASDs are well tolerated in infancy and
may spontaneously close, elective repair
frequently has been deferred until the child is
at least 4 years of age.
Is some patients with very large ASDs, closure is
done at younger ages.
There is no advantage in delaying repair much
beyond this age, and there may be harm in
delaying repair to the teenage years and beyond.
Spontanious closure of other types of ASDs is
not possible and must be closed surgically if
indicated.
Commen atrium usually must be repaired in
infancy because the most of them present
with symptoms of excess pulmonary blood
flow,fatigue,tachypnea and failure to thrive.
Ventricular
Septal Defect
Perimembranous: most common defect, 80% of surgical and autopsy
series; usually extends into muscular, inlet, or outlet areas
(synonyms: infracristal, membranous)
Outlet: 5%-7% of autopsy and surgical series (29% in the Far East),
situated just beneath the pulmonary value (synonyms: supracristal,
conal, infundibular, subpulmonary, doubly committed subarterial)
Inlet: 5%-8%, posterior and inferior to perimembranous defect
Muscular: 5%-20%
– Central: mid-muscular, may have multiple apparent channels on RV
side and coalesce to single defect on LV side
– Apical: multiple apparent channels on RV side may be single defect on
LV side as with central defect
– Marginal: along RV septal junction
– Swiss cheese•septum: large number of muscular defects
• In infants with small VSDs, a murmur usually is
detected at 1 to 6 weeks of age. However, the
murmur can be heard during the first days of life
associated with a rapid decrease in pulmonary
vascular resistance. With small defects, the
clinical course is benign throughout infancy and
childhood. There are normal patterns of feeding,
growth, and development. The only risk is that of
endocarditis, which is rare before the age of 2
years.
In some patients, the murmur can extend
cephalad along the left parasternal region,
owing to ejection across the outflow tract of
the right ventricle. The murmur also can
radiate to the right of the sternum. In children
with an outlet defect, the murmur and thrill
can be maximal at the second left intercostal
space or suprasternal notch.
Infants with moderate or large VSDs may develop
symptoms as early as 2 weeks of age. The initial
symptoms consist of tachypnea with increased
respiratory effort, excessive sweating owing to
increased sympathetic tone, and fatigue when
feeding. The infant progressively tires with
feeding; this symptom begins during the first
month and increases in severity as pulmonary
vascular resistance decreases. Symptoms occur
earlier in the premature than in the full-term
infant.
It is not unusual for symptoms to be preceded
by respiratory infection. This complication
makes it difficult to clarify the degree to which
the respiratory distress is due to heart failure
from a large left-to-right shunt versus
infection. In the absence of infection, the
cardiovascular basis for the respiratory
symptoms probably is pulmonary edema .
In infants with a large left-to-right shunt
secondary to a VSD, dyspnea can occur with
mean left atrial pressures slightly lower than
15 mm Hg .
In the presence of large shunts across the VSD,
infants often have normal length and
decreased weight.
In children with large shunts for ≥4 to 6
months, the left anterior thorax bulges
outward. Persistent cyanosis from birth
indicates a more complicated lesion than
isolated VSD. However, the occurrence of
cyanosis after infancy suggests reversal of the
shunt to right to left because of progressive
pulmonary vascular disease or the
development of significant infundibular
pulmonary stenosis.
Those with moderate to large right-to-left
shunts will be cyanotic at rest. This is rare in
infants, is occasionally seen by the age of 2 to
3 years, and is frequently seen in the
adolescent and young adult. The eponym
Eisenmenger's complex is now applied to the
condition characterized by a VSD with marked
elevation of pulmonary vascular resistance
and a predominant right-to-left shunt .
Indications for VSD closure:
1-Uncontrolled CHF including growth failure or
reccurent respiratory infections.
2-Elevated PAP even in the absence of
symptoms.Repair must be done before 2 years of
age and often before 1 year of age.
3-QP/QS >2
4-Significant dilation of LV
5-Aortic insufficiency
Pulmonary vascular obstructive changes can
occur as early as 2 years of age.
Generally, infants with VSD and increased
pulmonary artery pressure should undergo
repair between 3 and 12 months of age.
Development of pulmonary hypertension is rare
(4%) as is sinus node dysfunction (4%) but
progressive aortic valve insufficiency is fairly
common (16%).
TOF
Thankful