Quid Refert, Dummodo non Desinas, Tardius Ire
CARDIOLOGY – CHD and Acquired heart dse
PEDIA
CONGENITAL HEART DISEASE (continuation)
CHD First thing to look at is if its acyanotic or non cyanotic.
If cyanotic, then it probably starts with the letter t. Truncus
arteriosus
TAPVR? Cyanotic type. Why? Because of the overriding of
the aorta.
Usually, in utero, the right ventricle is dominant. Paglabas
ng bata, unti unting nagbabago depending on the
pulmonary pressure.
So in congenital heart disease, the most common type is
your acyanotic type which is your vsd (35%). In the
cyanotic type, you have the TOF.
Sa states, pareho lang ang prevalence ng PDA saka ASD.
Sa pilipinas, by census, mas marami ang PDA. Bakit
kaya? Because of the heart sounds. Madaling malaman
ang heart sounds ng PDA. In asd, ang titignan mo is the
size of the hole Sa ASD, pag maliit, wala kang masyadong
madidinig. Minsan wala. Sa states, nasasabi nila na asd
because of the autopsy. Sa philippines, hindi
pinapaautopsy lahat. No matter how toxic the patient is or
no matter how bad the patients condition, as long as the
relatives did not agree, you cannot do an autopsy.
What are the reasons kung bakit hindi agad nadidiagnose
ang congenital heart disease? Because of the symptoms.
Pag walang symptoms, hindi pinapatignan ng magulang.
Hindi naman daw nangingitim ang anak nya saka di
naman daw napapakinggan yung sinasabi ni Dra. E
pinapakinggan nyo po ba sa center? Pinapabakunahan
lang daw. Hindi naman na PE ng mga doctor sa center
yung bata kaya walang napapakinggan. Plus, ang
magulang, ang notion nila, pag hindi nangingitim, walang
sakit sa puso. Mali.
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DRA ESGUERRA
Sometimes you do not hear a sound. Minsan yung nanay
nagrereklamo kasi nanganak naman daw sya sa ospital
tapos sasabihin ng pedia na may sakit daw sa puso ang
anak nya ngayong 2 months na sya. Bakit di nya narinig
na may sound? In cases like this, you have to explain sa
magulang na pwedeng walang marinig. Would you believe
na I have a patient, isang taon nang regular patient ko,
saka ko lang narinig na may murmur. I see the patient
every month. Nung mag iisang taon na, naririnig kong may
sounds. Bakit kaya? What im sure of is, walang butas.
Kasi its not a sound of a butas. Sabi ko, sige silipin natin.
My gosh meron syang coronary artery stenosis. Kaya hindi
marinig kasi wala pang obstruction. So I told the parents
na possibleng operahan ang bata at possible ding
mamatay ang bata.
The hemodynamic appearance of the fetal circulation.
Hanggat mataas ang pulmonary pressure, wala kang
mariring dyan kung PDA yan. Remember? The murmur is
not continuous. Kasi mataas pa ang pressure sa baga.
The size of the defect - pag maliit ang defect, wala kang
masyadong maririnig. Plus if you do not have situs
inversus, may ibang pasyente, sasabihin, ngayon 6 na
taon na ang anak ko tapos sasabihin nyo may sakit sa
puso? Who knows kim? Si matang lawin. Ilang taon na
nung nalaman nyang may sakit sya sa puso? Mag 40 na
diba? Okay naman sya from the start. Na stroke lang sya
mga 2011 ata. O bakit sya nag stoke? Lahat naman
normal. Yun pala, meron syang patent foramen ovale.
_________________ circulation. So what are the causes?
You may have trisomy, conotruncal lesion, branchial arch
defects, dilated cardiomyopathy - 2 types: acquired and
congenital, brugada syndrome (bangungot) - they say that
pag bigla kang namatay during sleep, you have daw
bangungot. But now, it is secondary to brugada syndrome.
Brugada syndrome - this is a very new illness. Merong
magkakapatid, the Brugada brothers from spain. Naka
hook sila sa ecg para makita yung abnormalies. Sad to
say, 100% ang mortality rate ng brugada. So nakikita
nalang nila na nagkakaroon ng abnormalities sa ecg. In a
normal patient, wala kang makikita sa ecg. Brugada has 3
types. In type 1, makikita mo, in a normal setting na may
konting abnormalities. In type 2&3, the ecg pattern is
questionably normal. Mahirap idistinguish ang abnormality.
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 Meron akong isang patient, 3 ang anak nya, they all have LVH
CHD and the all died. Kaya pag ganun wag na kayong
Vsd
mag produce.
Pda

Avsd
Categories of congenital heart disease: Acyanotic
Cyanotic - most of the times, starts with the letter t. RVH

Asd – may also have lvh

Shunt anomalies Tapvr-
Asd Tatvr
Pda Eisenmeger’s phenomenon, hindi na kasama yan
Vsd Under your shunt anomaly, this is the only one that may
have ___ similarities.
Avsd

Alam na natin kung ano yung 3. Pero ano yung avsd?

Atrioventricular septal defect. It may have an asd and a
vsd ( incomplete type)
Volume overload
Acyanotic type
Valvular regurgitation
Dilated cardiomyopathy
You have your right and left tract; ang normal ratio is 1;1.
The amount of blood that goes into the pulmonary (lungs)
Qs ; amount of blood that goes into the systemic
circulation. Kapag nagging 2:1 yung ratio, ibig sabihin
increased yung pressure sa pulmonary circulation mo, and
that is abnormal.
Avsd may have LVH, all of the above will go into
eisenmegers phenomenon. What is an eisenmegers
phenomenon? Ibig sabihin, you have LVH, and then lahat
sila, magkakaroon ng RVH. All of them. Why? Because
they have increased pulmonary pressure so they will go
into pulmonary hypertension. If you auscultate those
patients with pulmonary hypertension, they have loud p2.
Remember that your heart sounds are divided into two.
Your s1 and s2. S2 is divided into 2, your a2 and p2. In
eisenmegers phenomenon, mataas and second heart
sound, mataas ang p2, loud ang p2. Plus, a patient who is
initially acyanotic would become cyanotic. So how would
you know if the patient is in eisenmeger? meron syang
loud p2, cyanosis, by history anong makikita mo? Meron
syang RVH, okay? So lahat sila asd, pda, vsd, tatvr, tapvr
they will all go into eisenmegers phenomenon. When you
say eisenmegers phenomenon, the patient is already in
pulmonary hypertension.

Pressure overload (Bara) – obstruction

Cyanosis ACQUIRED HEART DISEASE

Atresia

Coartation of the aorta Give me an example of your acquired heart disease (other
than your rheumatic heart disease myocardial infarction?
Pwede. Infective endocarditis, ano pa? dilated
Patient with heart failure  incrased in cathecolamine cardiomyopathy.very good, ano pa? congestive heart
production  tachycardia failure, hypertension, pwede sa bata, ate, ano?
Hypertrophic cardiomyopathy, restrictive cardiomyopathy,
myxoma – most of the time, that is congenital kaya lang,
lately diagnosed., pericardial effusion, pericarditis. So your
pericarditis can occur in a normal heart and in an abnormal
Obstruction
heart. So sino kaya ang pasyente and prone na

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 magkaroon ng infective endocarditis? Severe infection,
sepsis pwede. Immunocompromised, enzyme deficiency,
trauma, invasive procedures like cardiac catherization, TB
(pwede), diabetes (pwede), basta immunocompromised
patient. Those on mechanical ventillators, staphylococcal
infection, valve replacement. Ano pa? normal ang puso
nya, anong procedure na ginagawa na pwede magkaroon
ang pasyente ng IE? Pericardiocenthesis, sa nursery, bakit
ang mga baby, laging pinapa 2d echo, pero septic ang
pasyente? Anong ginagawa nila sa baby? Cord clumping?
Malapit na dun. Anong ginagawa sa umbilical cord nila?
Nag uumbilical catherization diba? That is a very strong
risk factor. Sa adults naman, anong ginagawa nila kaya
nagkakaroon sila ng IE? Mga drug users. Kasi they don’t
care kung gamit na ang needle. Yung may mga piercing,
pwede magkaroon. Kasi merong tongue device na
nagpenetrate na sa skin so pwede un. Kapag ang ginamit
mo ay nonsterile, pwede magkaroon.
Those who are not high risk, of ages 2-15 years,
congenital is still the highest. For those who are 50 – 60
y/o, common ang rheumatic. So ang rheumatic, kaya tayo
nagbibigay ng prophylaxis is that because we are afraid of
infective endocarditis. Kasi, when a patient has IE, you
have to treat that for 4 weeks- 6 weeks.
If have a preexisting congenital heart disease or acquired
heart disease, there is an abnormality in the flow. Normally,
ang flow is laminar, but in these cases, turbulent yung
blood flow. There is less resistace if laminar. If you have
an increase in pressure, you will now have your turbulence
We have one patient sa heart center, hindi ko sya
makalimutan, kasi he is diagnosed with TAPVR, nung nag
ka IE sya, tinamaan yung kanyang arm, kaya we have to
amputate the arm.
So how to you diagnose IE?
There has to be a new murmur
There has to be a positive echocardiograph – it is one of
the major criteria.
There are only two major criterias, your echocardiograph
and your blood culture.
So pag nag sample ka ng blood, dapat 2-3 samples over
24 hours. Pag walang kamay at walang paa, sa singit mo
kunin ung sample. Pag hindi pwede sa singit, san ka
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kukuha? Sa jugular. E pag may nakalagay na sa jugular
nya? San pa tayo pwede kumuha? May Amelia ung
pasyente, walang kamay at walang paa. We have a
patient in the ICU ngayon, para syang naburn, kusang
naaamputate ang kanyang mga limbs. Ngayon wala ng
makuhaan. So we have to use the jugular. Okay pa naman
ung line, pero ngayon, di na sya pwede kuhaan doon.
Newborn ung pasyente, hindi pa nila ma open up. So san
mo pa sya pwedeng kuhaan? Sa temporal? Grabe naman.
San pa ba pwede, maliban sa temporal at maliban sa
jugular. May nakasuksuk nga sa jugular kaya hindi pwede
e. So saan? Sa heart? Mas lalong hindi pwede. Edi kunin
mo sa Axilla.
One of the acute phase reactants, mejo elevated, your
ESR and your ____ protein factor?
Patient may have anemia, secondary to hematuria
You may have leukocytosis
Patient may have elevated antibodies
Under the criteria mentioned, you have your
echocardiogram and your blood cultures, so to diagnose,
you have to have 2 major and 1 minor or 1 major and 3
minor or pag wala kang major, dapat meron syang 5 minor.
Prognosis – patient may have heart failure. Kaya ang mga
pasyente dapat nasa hospital. We have one patient in
heart center, I was a fellow then, nagkaroon sya ng
sinus____itis. Hindi ko alam, kung bakit, kamalas,
malasan, yung kanyan VSD kasi is subaortic, ibig sabihin
malapit sa aortic valve. Sumakay sa tricycle ung bata at
nagkaroon sya ng IE. Nadischarge ung pasyente still,
meron pa rin syang infection. Nakumpleto nya ung 4
weeks na antibiotics. Sumakay ung pasyente ng tricycle,
hindi ko alam, napakamalas nya, nalaglag yung bata at
natanggal yung kanyang shunt dun sa coronary artery nya,
patay yung bata. Okay so delikado yan. Etong batang to
napakamalas, yung thrombus?? Napunta dun sa coronary
artery nya. Ewan ko ba, di ko alam kung bakit ganun sya
kamalas.
Pag may IE ang patient, you have to give ceftriaxone plus
gentamycin, for 4 weeks. If the patient is resistant for
penicillin then give vancomycin. When I had this patient,
what I did is I referred the patient to dra. Fajardo and she
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 gave linezolid. Ang vancomycin mo, nasa 2k, mas mahal
ang linezolid. The tablet costs about 6k. however hindi
kaya, ang ending, mamamatay din ang bata.

ACQUIRED HEART DISEASE

 Bacterial Agents in Pediatric Infective Endocarditis

o COMMON: NATIVE VALVE OR OTHER CARDIAC LESIONS
o Viridans group streptococci (S. mutans, S. sanguis, S. mitis)
o Staphylococcus aureus
o Group D streptococcus (enterococcus) (S. bovis, S. faecalis)

INFECTIVE ENDOCARDITIS  UNCOMMON: NATIVE VALVE OR OTHER CARDIAC LESIONS

o Streptococcus pneumoniae
 Infective endocarditis is a microbial infection of the endocardial o Haemophilus influenzae
(endothelial) surface of the heart. o Coagulage-negative staphylococci
o Native or prosthetic heart valves o Coxiella burnetii (Q fever)[*]
o Endocarditis also can involve septal defects o Neisseria gonorrhoeae
o The mural endocardium o Brucella[*]
o Intravascular foreign devices o Chlamydia psittacli[*]
 intracardiac patches o Chlamydia trachomatis[*]
 surgically constructed shunts o Chlamydia pneumoniae[*]
 intravenous catheters. o Legionella[*]
 Infective endocarditis is a microbial infection of the endocardial o Bartonella[*]
(endothelial) surface of the heart. o HACEK group[†]
 Native or prosthetic heart valves are the most frequently involved sites. o Streptobacillus moniliformis[*]
 Endocarditis also can involve septal defects, the mural endocardium, or o Pasteurella multocida[*]
intravascular foreign devices such as intracardiac patches, surgically o Campylobacter fetus
constructed shunts, and intravenous catheters. o Culture negative (6% of cases)

 PROSTHETIC VALVE
o Staphylococcus epidermidis
o Staphylococcus aureus
o Viridans group streptococcus
o Pseudomonas aeruginosa
o Serratia marcescens
o Diphtheroids
o Legionella species[*]
o HACEK group[†]
o Fungi[‡]

PATHOGENESIS

ETIOLOGY

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 LABORATORY DIAGNOSIS

 most valuable tool

 Collection of 2 or 3 samples over a 24 hr period is adequate in most cases
 Acute phase reactants are elevated
 ESR – only minimally elevated (as the disease progresses , the ESR will
increase)
o remain elevated for some time even after documented
bacteriologic cure
 Immune complexes or Rheumatoid factor
 Anemia – common, particularly in long standing infection
o May be hemolytic or may represent anemia of chronic disease
 Microscopic or macroscopic hematuria represents renal embolization or
nephritis
 Leukocytosis – is not a consistent finding but is more common in acute IE
 Antibodies against techoic acid and cell wall peptidoglycan in severe
staphylococcal infection may be present

2D- ECHOCARDIOGRAPHY

 A negative echocardiogram does not rule out endocarditis

 More helpful in children with normal cardiac anatomy or with isolated
valvar abnormalities in children with more complex congenital anomalies
Clinical and Laboratory Findings in Patients with IE  Duke Major Criteria : oscillating intracardiac mass or vegetation, an
annular abscess, prosthetic valve partial dehiscence, and new valvular
Finding Frequency regurgitation
Clinical
o Fever ++++ DIAGNOSIS
o Non-specific symptoms
(myalgia, arthralgia,
 Duke criteria
headache, malaise) +++
 Major:
o Heart murmur (new or changing ++
o (+) blood culture
o Heart Failure ++
o Evidence of endocarditis on echocardiography
o Petechiae ++
A. Positive echocardiogram for IE defined as:
o Embolic phenomena ++
i. Oscillating intracardiac mass on valve or supporting
o SplenomegalY ++
structures, in the path of regurgitant jets, or an implanted
o Neurologic Findings ++
material in the absence of an alternative anatomic explanation
o Osler nodes, Janeway lesions,
or
Roth spots, splinter hemorrhages +
ii.Abscess, or
iii.New partial dehiscence of prosthetic valve or
Legend:
B. New valvular regurgitation (worsening or changing of preexisting
++++ very common ++ infrequent
murmur)
+++ in most cases + rare
 Minor criteria
o Predisposition: predisposing heart condition or intravenous drug use
Finding Frequency
o Fever: temperature > 38.0° C (100.4° F)
Laboratory
o Positive blood culture o Vascular phenomena: major arterial emboli, septic pulmonary
infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival
(off antibiotics) ++++
hemorrhages, and Janeway lesions
o Elevated acute phase reactants ++++
o Anemia +++ o Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth’s
spots and rheumatoid factor
o Hematuria +++
o Presence of rheumatoid factor ++ o Microbiological evidence: positive blood culture but does not meet a
major criterion as noted above¹ or serological evidence of active
o Leukocytosis ++
infection with organism consistent with IE
Legend: o Echocardiographic findings: consistent with IE but do not meet a
major criterion as noted above
++++ very common
+++ in most cases o Excludes single positive cultures for coagulase-negative
staphylococci, diphtheroids, and organisms that do not commonly
++ Infrequent
cause endocarditis.
+ rare
 DIAGNOSIS
CLINICAL FEATURES
o 2 major criteria or
o 1 major and 3 minor criteria or
 new or changing murmurs are usually heard
o 5 minor criteria
o Frequent auscultation is essential
 Patients with suspected embolic events are candidates for serial echo to
PROGNOSIS AND COMPLICATIONS
localize vegetations and to define changes that may occur with time
 Heart failure-mitral and aortic valve
 Splenomegaly may be present in a majority of instances when the disease
has been present for weeks or months  Myocardial abscess and toxic myocarditisArrhythmias
 Neurologic findings are present in 20% of children and may simulate the  Systemic emboli
picture of an abscess, infarct or aseptic meningitis  Pulmonary embolism VSD TOF
 mycotic aneurysms

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  rupture of a sinus of Valsalva, obstruction of a valve secondary to large
vegetations, acquired VSD, and heart block as a result of involvement
(abscess) of the conduction system.
 meningitis, osteomyelitis, arthritis, renal abscess, and immune complex–
mediated glomerulonephritis.

TREATMENT

RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE

 Definition:
o An auto immune disease preceded by GABS
o Generalized disease affecting all the connective tissues of the
body
o Characterized by periods of exacerbation
o Commonly affects 6-15 years old

DIAGNOSTIC CRITERIA

 Major Criteria
1. Arthritis
2. Carditis
3. Erythema Marginatum
4. Subcutaneous nodules
5. Chorea

Diagnosis
2major
1major + 2minor

WITH PROSTHETIC VALVES OR PROSTHESIS CAUSED BY STREP VIRIDANS BUT

PENICILLIN RESISTANT

AHA Guideline 2008

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