case ll real)
TRANSCRIPT
Subjective data
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ประวั�ติ�ป�จจ�บั�น : ทาร็กเพศหญิ!งอาย" 3 เดู�อนื่มาร็ดูาพามาปร็�กษาแพทย%ดู&วยอาการ็หายใจเร็ว เหนื่��อยมากขึ้��นื่เวลาดู�ดูนื่ม เหง��อออกมาก ดู�ดูนื่มไดู&นื่&อย นื่(�าหนื่)กตั)วเพ!�มขึ้��นื่เพ+ยงเลกนื่&อย ไม�ม+ไขึ้& ไอเป,นื่บางคร็)�ง อาการ็เป,นื่มากขึ้��นื่เร็��อยๆในื่ช่�วง 1 เดู�อนื่ จ�งมาปร็�กษาแพทย%
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Problem lists
• Dyspnea (exertional dyspnea)
• Difficulty with feeding
• Tachypnea
D yspnea : Difficult or labored breathing
Definition
Exertional dyspnea :Dyspnea provoked by physical effort or exertion
Ref.: Douglas M., Anderson.Dorland’s illustrated medical dictionary. 28th ed.philadelphia:W.B Saunders Co.,1994.
Tachypnea :
Abnormally fast breathing. A respiratory rate that is
too rapid. The normal rate of respirations (breaths per minut
e) depends on a number of factors, including the age of the i
ndividual and the degree of exertion.
Pathophysiology of dyspnea
Dyspnea
Increase pulmonary resistance
Pulmonary congestionor pulmonary edema
Decrease lung compliance
Decrease gas exchange
Difficult feeding
Difficult breathing
Dyspnea
Parenchymal lung disease
Pulmonary dyspnea
Obstructive disease of airway
Congenital
Cardiac dyspnea
• Pneumonia
Acquire
URT LRT
• Asthma
• Aspiration of
foreign body
• Allergic history
• Bronchiolitis
•Cardiomyopathy
• CAD
obstruct
Rt to Lt • TOF
Lt to Rt• ASD• VSD• PDA
shunt
Pulmonary stenosis
Tachypnea
AgeRespiratory
rate(bpm)
Premature 40-70
0-3 months 35-55
3-6 months 30-45
6-12 months 25-40
Ref. : Behrman, Nelson Textbook of Pediatrics : 17th edition. * From Dieckmann R, Brownstein D, Gausche-Hill M (eds ): Pediatric Education for Prehospital Professionals . Sudbury, Mass, Jones & Bartlett, American Academy of Pediatrics, 2000, pp 43-45 . From American Heart Association ECC Guidelines, 2000.
Tachypnea
Decrease gas exchange
High Pco2, high [H+], low Po2
Respiratory center (medulla)
Tachypnea
Tachypnea
• Pulmonary etiologies
- Pneumonia
- Pneumothorax
• Cardiovascular etiology - CHF
• Metabolic acidosis
- Drug : Aspirin
Subjective data
อาการสำ�าคั�ญ : หายใจเร็วและเหนื่��อยมากขึ้��นื่เวลาดู�ดูนื่ม 1 เดู�อนื่ก�อนื่มาโร็งพยาบาล
ประวั�ติ�ป�จจ�บั�น : ทาร็กเพศหญิ!งอาย" 3 เดู�อนื่มาร็ดูาพามาปร็�กษาแพทย%ดู&วยอาการ็หายใจเร็ว เหนื่��อยมากขึ้��นื่เวลาดู�ดูนื่ม เหง��อออกมาก ดู�ดูนื่มไดู&นื่&อย นื่(�าหนื่)กตั)วเพ!�มขึ้��นื่เพ+ยงเลกนื่&อย ไม�ม+ไขึ้& ไอเป,นื่บางคร็)�ง อาการ็เป,นื่มากขึ้��นื่เร็��อยๆในื่ช่�วง 1 เดู�อนื่ จ�งมาปร็�กษาแพทย%
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ทารกคัลอดีก�อนก�าหนดีเมื่��ออายุ�คัรรภ์!ไดี# 35 สำ�ปดีาห!
• Preterm infant : before 37 wks.
• Post term infant : after 42 wks.
• Pulmonary immaturity–surfactant deficiency is associated with structural immaturity in infants younger than 26 weeks' gestation. This condition is complicated by the combination of noncompliant lungs and extremely compliant chest wall, causing inefficient respiratory mechanics.
• Persistent patency of the ductus arteriosus compromises pulmonary gas exchange because of overperfusion
• Immature cerebral vasculature and structure predisposes to subependymal or intraventricular hemorrhage and periventricular leukomalacia.
• Impaired substrate absorption by the GI tract compromises nutritional management.
• Increased susceptibility to infection.
THE PRETERM INFANT
Subjective data
อาการสำ�าคั�ญ : หายใจเร็วและเหนื่��อยมากขึ้��นื่เวลาดู�ดูนื่ม 1 เดู�อนื่ก�อนื่มาโร็งพยาบาล
ประวั�ติ�ป�จจ�บั�น : ทาร็กเพศหญิ!งอาย" 3 เดู�อนื่มาร็ดูาพามาปร็�กษาแพทย%ดู&วยอาการ็หายใจเร็ว เหนื่��อยมากขึ้��นื่เวลาดู�ดูนื่ม เหง��อออกมาก ดู�ดูนื่มไดู&นื่&อย นื่(�าหนื่)กตั)วเพ!�มขึ้��นื่เพ+ยงเลกนื่&อย ไม�ม+ไขึ้& ไอเป,นื่บางคร็)�ง อาการ็เป,นื่มากขึ้��นื่เร็��อยๆในื่ช่�วง 1 เดู�อนื่ จ�งมาปร็�กษาแพทย%
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The effects of primary maternal rubella infection on the fetus are dependant on the
time of infection
• First 2 months : 90% fetal damage , 1% or more severe
defects or spontaneous abortion
•3rd month : 30-35% most likely single defect such as deafness, congenital heart disease
•4th month : 10% single congenital defects
• 17 + weeks defects rarely encountered. Occasional deafness up to 20 weeks
• Maternal reinfection - fetal damage rare
Congenital rubella syndrome
• Most common : triad
• Heart defects : PDA (most common), PS
• Deafness
• Retinopathy / Cataracts
• Less common
• Intrauterine growth retardation
• Thrombocytopenic purpura
• Hepatosplenomegaly
Ref: Park MK. Pediatric cardiology for Practitioners 4th ed.,2002.
Conclusion from subjective data
TachypneaDyspnea on exertion
Difficulty feedingRubella
CVSRS
Preterm
CVSRS
• Abnormal breath
sound
• Cyanosis
• Alterations in the
pattern of breathing
• Murmur
(PDAcontinuous
murmur)
• Cyanosis
• Dyspnea
• Tachypnea
•
Tachycardia/bradycardia
• Edema
From problem lists and maternal history
Suspect
Congenital heart disease
Physical
examination!!!
Physical Examination
Which Systems are
involved?Results?
Vital sign: Body temperature
Respiratory Rate
Blood Pressure
Heart Rate
normal? infection?
dyspnea? heart disease?
???
heart disease?
Heart : Heart sound
Heart murmur
S3? S4?
systolic, diastolic, continuous
murmur
Lung crackles?
Others pale? cyanosis?
Vital sign : BT 37 , BP 95/45 mmHg, PR 160/min, RR 50/min with chest retraction
GA : crying, dyspnea, not pale, no cyanosis
HEENT : within normal limit
Heart : sinus tachycardia, continuous murmur grade 3/6 at parasternal area of second left intercostal space.
Lung : fine crackles both lower lung fields.
Abdomen : hepatomegaly
Extremities : Bounding pulse of extremities.
C
Physical examination
Vital sign
Normal value
Physical examination value
Results
BT 36.4-37.4 oC 37 oC Normal
BP70-95/60-90
mmHg95/45 mmHg
Wide pulse pressure
PR100-120
bpm160 bpm Tachycardia
RR 30-45 tpm 50 tpm Tachypnea
Vital sign
(infant age 1-12 months)
Ref.: Emergency Care and Transportation of the Sick and Injured, EMS Field Guide and Journal of Emergency Medic alSer vi ces.
Chest wall retraction
Increased respiratory effort may be appeared by
increased respiratory rate, increased chest wall excursion, and
retractions of
the less rigid structures of the thorax.
Retractions of the sternum, suprasternal notch and
intercostal retractions reflect increased respiratory effort.
This may be due to obstructive disease such as asthma
or tracheal obstruction, pneumonia, or restrictive disease.
Clip -- Infant
Wide pulse pressure in infant
Wide pulse pressure: Difference between systolic and
diastolic BP
more than 25 mmHg so increased
hemodynamic flow followed.
- increased systolic BP and decreased diastolic BP e.g. dynamic
exercise
- increased systolic BP and normal diastolic BP e.g. static
exercise
- normal systolic BP and decreased diastolic BP e.g. PDA
Bounding pulse : a forceful and strong pulse.
Bounding pulse of extremities
Ref.: The Indian Journal of prediatrics, volume 75:number 3, 2008.)
Sinus tachycardia
A fast heartbeat (tachycardia) because of rapid firing of
the sinoatrial (sinus) node. The sinoatrial (or sinus) node is the n
atural pacemaker of the heart. It is located in the wall of the righ
t atrium (the right upper chamber of the heart). Ref.: http://www.cardiologymedley.com/journals/VTIHD.pdf
Ref.: - Park MK. Pediatric cardiology for practitioners. 3 ed. New York: Mosby Year 1996book; .
Clinical Correlations :
- Hypoxia or AMI (after hypoxia, sympathetic hyperreactivity
occurs)
- Exertion (stimulate sympathetic nervous system)
- Fever (increased metabolism)
- CHF (increased contractility)
Murmur
Murmur, or bruit, are abnormal sounds heard in various parts of the vascular system. Above the critical velocity, and beyond an obstruction, blood flow is turbulent instead of laminar . Laminar flow is silent, but turbulent flow creates sounds .
Heart Sounds :
S1 is the sound of closure of mitral and tricuspid valves.
S2 is the sound of closure of aortic and pulmonary valves.
S3 is the sound of early diastolic filling.
S4 is the sound of late diastolic filling.
1. Systolic murmur (systolic phase) occurs between the S1 and S2
- Systolic ejection murmur caused by the flow of blood through stenotic or deformed semilunar valves or by increased flow through semilunar valve. These murmurs are generally crescendo-decrescendo or diamond-shaped.
- Pan systolic murmur caused by flow of blood from chamber that is at a higher pressure thoughout systole than the receiving chamber associated with VSD, MR, tricuspid regurgitation.
Classifications
2. Diastolic murmur (diastolic phase) occurs between the S2 and S1
- Diastolic blowing murmur caused by incompetent of aortic and pulmonary valve. Decrescendo murmur occur early in diastole; immediately after the S2.
- Diastolic rumbling murmur are heard in early or middiastole. These murmurs are always low pitched. They caused by turbulence in to mitral or tricuspid valve secondary to anatomic stenosis.
3. Continuous murmur (systolic and diastolic phase)
Begin in systole and continue without interruption through the S2 into all or part of diastole. Continuous murmur are caused by the following:
1. Aortopulmonary or arteriovenous connection (e.g. PDA, AV fistula, after systemic-to-PA shunt to surgery)
2. Disturbance of flow patterns in veins (e.g. venous hum)
3. Disturbance of flow patterns in arteries (e.g. COA, PA stenosis)
Ref.: - 3Park MK. Pediatric cardiology for practitioners. ed. New York: Mosby Year book;
1996.
LINK file record murmur
Listening Areas for Common Pediatric Heart Murmurs
Ref.: http://www.aafp.org/afp/990800ap/558.html
PDA
PS
ASD
MRVSD
TR
AS
Area Murmur
Upper right sternal
border
Aortic stenosis, venous hum
Upper left sternal border Pulmonary stenosis, pulmonary flow
murmurs, atrial septal defect, patent
ductus arteriosus
Lower left sternal border Still's murmur, ventricular septal
defect, tricuspid valve regurgitation,
hypertrophic cardiomyopathy,
subaortic stenosis
Apex Mitral valve regurgitation
Listening Areas for Common Pediatric Heart Murmurs
Gradations of murmurs
graded according to their intensity (loudness)
Fine crackles both lower lung fields
Crackles or rales or crepitations :
Abnormal breath sounds are usually caused by excessive fluid
within the airways. This fluid could be due to an exudate, as in pneumoni
a or other infections of the lung, or a transudate, as in congestive heart fa
ilure . You will notice that crackles sound just as they are named, and are t
ypically inspiratory. The crackles in this example are particularly wet sou
nding, with dry crackles sounding more like rubbing hair together next to
your ear or like the sound of opening Velcro.
Ref.: http://www.wilkes.med.ucla.edu/cracklesmain.htm
Hepatomegaly
• Congestive heart failure esp. right side
(systemic venous congestion)
• Hemolytic anemia (increased hepatic
function)
• Hepatitis viral infection (inflammation)
• Leukemia (increased hepatic function)
Ref.: http:// www.nlm.nih.gov/medlineplus/ency/artide/003275.htm
From problem lists, history, and physical examination.
Suspect
“Congestive Heart Failure”
due to
Patent Ductus Arteriosus
LAB
Diagnosis & Management :
• Chest X-ray
•
Echocardiograph
y
•
Electrocardiogra
m
Lab investigation
Size , Pulmonary vasculature
Diameter , length, tortuosity of PDA
Management : CBC
Left atrium and ventricle hypertrophy
CBCNormal values
Laboratory values
Result
Hct (%) 31-41 33 Normal
Hb (gm%) 9.5-14.5 11 Normal
WBC (cell/mm3) Neutrophil Lymphocyte Monocyte Eosinophil Basophil
6,000-18,00057-6725-333-71-30-1
85006525541
Normal
MCV (fL) 70-86 78 Normal
MCH (pg) 30-36 26 Normal
MCHC (%) 25-35 31 Normal
Platelet (/mm3) 150,000-400,000 120,000 Normal
Ref : Behrman, Nelson Textbook of Pediatrics : 17th edition.
Chest X-ray
Normal
• Moderate cardiomegaly
• Left ventricular
hypertrophy
• Prominent aortic knob
• Prominent main
pulmonary
artery with increase
pulmonary vasculature
Chest X-ray
Cardiothoracic Ratio
CT ratio = (A + B ) ÷ C >0.5 indicate cardiomegaly
Case : CT Ratio = 0.54
Ref.: Myung K. Park, Pediatic Cardiology For Practitioners; 1996.
• Moderate cardiomegaly
• Left ventricular
hypertrophy
• Prominent aortic knob
• Prominent main
pulmonary
artery with increase
pulmonary vasculature
Chest X-ray
PDA vs CASEPDA Case
Right atrium N N
Right ventricle N N
Pulmonary artery
Pulmonary vascularity
Left atrium N / -
Left ventricle N /
Cardiac size
Aorta
Ref.: กฤษฎี+ ปร็ะภ์าสัะว)ดู . ร็)งสั+ว!นื่!จฉั)ย คณะแพทย%ศาสัตัร็%ศ!ร็!ร็าช่พยาบาล . บร็!ษ)ท ท+ซี+จ+ พร็!�นื่ตั!�ง จ(าก)ดู; กร็"งเทพฯ , 2546
Echocardiography
• A test that uses sound waves to creat
e a moving picture of the heart
• The picture is much more detailed th
- an X ray image
• I nvolves no radiation exposure
Echocardiography
Ref.: http://www.fi.edu/learn/heart/monitor/echo.html&usg
Echocardiography
• Left atrial and left ventricular
enlargement
• Patent ductus arteriosus 5 mm.
PDA
Basic sciences
• Mesoderm ร็อบๆ endocardial heart tube MyocardiumMyocardium • Mesothelial cell จาก Sinus venosus EpicardiumEpicardium
Primitive heart tube Primitive heart tube : Endocardium + Myocardium + Epicardium
- Begin in 3rd week
Development of the Heart
• Splanchnic mesodserm Splanchnic mesodserm
Angiogenic cell cluster Endocardial heart tube (2
tube)
Single Endocardial heart tube EndocardiumEndocardium
- Primitive heart tube ขึ้ยายออกเป,นื่ 5 สั�วนื่
Truncus arteriosus
Tetralogy of Fallot
Aorticopulmonary septum
- Primitive heart tube ขึ้ยายออกเป,นื่ 5 สั�วนื่
Truncus arteriosus
- Truncus arteriosus - Proximal part of aorta
- proximal part of pulmonary
trunk
- Bulbus cordis - Smooth part of right ventricle
- Smooth part of left ventricle
- Primitive ventricle - trabeculated part of right ventricle
- trabeculated part of left ventricle
- Primitive atrium - trabeculated part of right atrium
- trabeculated part of left atrium
- Sinus venosus - Smooth part of right atrium
- Coronary sinus
- Oblique vein of left atrium
Foramen secondum
Septum primum
Foramen primum
Endocardial cushion
Septum primum
Septum secondum
Foramen ovale
Septum primum
Foramen secondum defect
Interventricular foramen
Muscular interventricular septum
Membranous interventricular septum
Ventricular septal defect
(VSD)
Endocardial cushion
Chordae tendineae
Papillary muscle
Atrioventricular orifice
- Tissue ย��นื่เขึ้&าไปในื่ช่�องว�างขึ้อง Aorta + Pulmonary artery
Cusp 3 แผู้�นื่ Aortic + Pulmonary semilunar
valve
Semilunar valve formation
• Umbilical artery : น�าเล�อดีออกซิ�เจนติ��า Placenta
• Aortic arch : จากสั�วนื่ปลายขึ้อง truncus arteriosus แตักแขึ้นื่งเป,นื่ 6 ค��และท+�บร็!เวณล(าตั)วเป,นื่ dorsal aorta
- Begin in 4th, 5th week
Development of theDevelopment of the Arterial vessel system
• Vitelline artery : น�าเล�อดีออกซิ�เจนสำ%ง Yolk sac
Aortic arch
Aortic arch คั%�ท�� 1 - Maxillary artery- External carotid artery
Aortic arch คั%�ท�� 2 - Hyoid artery- Stapedial artery
Aortic arch คั%�ท�� 3 - Common carotid artery- Internal carotid artery
Aortic arch คั%�ท�� 4 - Arch of Aorta- Right subclavian artery
Aortic arch คั%�ท�� 5 สัลายไป
Aortic arch คั%�ท�� 6 - Left pulmonary artery- Ductus arteriosus- Right pulmonary artery
Ductus arteriosus
Lt. pulmonary artery
Dorsal aorta
Fetal circulation
Ref.: The McGraw-Hill Companies. All rights reserved.CURRENT OB/GYN> Chapter 32. The Resuscitation & Care of the Newborn at Risk>
1. Foramen ovale Fossa ovalis
respirations initiated & fluid in lung absorbed
PVR , PBF
Pulmonary venous return to left atrium
Left atrium มื่� pressure > Right atrium
foramen ovale closed
Postnatal circulation
2. ductus venosus ligamentum venosum
Cramps umbilical cord
Systemic vascular resistance
Cessation of umbilical venous return
Closure of ductus venous
• 3. Ductus arteriosus ligamentum arteriosum
Cramps umbilical cord
systemic vascular resistance more than pulmonary resistance
Aortic blood pressure PBF
Oxygenated blood pass ductus arteriosus to pulmonary artery
constrict smooth muscle of DA PGE2
DA Closed
• Functional closure,almost within 10-15 hr. in full-term infant by smooth muscle
constriction (If the murmur occur after 96 hr. after birth Abnormal closure)
• Anatomical closure completely within 2-3 wk. due to extensive neointimal
thickening and loss of smooth muscle cells from the inner muscle media.
Factor that enchance closing of DA
• oxygen, PGE2, maturity of
the newborn, ACh,
bradykinin
Ref.: - 3 1996Park MK. Pediatric cardiology for practitioners. ed. New York: Mosby Year book; .
65%
65%
99%
Risk Factors of PDA
• Rubella infection in 1st trimester
• Preterm labor
• High altitude area
• Substances eg. Alcohol
• Respiratory distress syndrome
Ref.: Park MK. Pediatric cardiology for Practitioners 4th ed.,2002. : ตั(าร็าก"มาร็เวช่ศาสัตัร็% เล�ม 1 ภ์าคว!ช่าก"มาร็เวช่ศาสัตัร็% คณะแพทยศาสัตัร็% โร็งพยาบาลร็ามาธิ!บดู+, 2542.
Rubella with congenital heart disease
• The rubella virus crosses the placenta and
spreads through the fetal circulatory system
damaging blood vessels by induce endothelial cell
apoptosis
• The rubella virus apparently interferes with the
normal formation of arterial elastic tissue, resulting
in patency of the ductus arteriosus and peripheral
pulmonary and systemic arterial stenosis
Congenital heart disease
Shunt Obstruction
Left-to-right shunt Right-to-left shunt
VSD
PDA
ASD
Tetralogy of fallot
Transposition of great arteries (TGA)
Persistent truncus arteriosus
Coarctation of aota
Pulmonary stenosis
Aortic stenosis
cyanosis
No cyanosis
Preload
Pathophysiology of PDA
Continuous murmur
BP
hypertrophy
Volume Volume OverloadOverload
hypertrophy
Starling’s law
Contractility
CO
Patent ductus arteriosus
Preload
Compensate
baroreceptor
RAA system
HR
contractility
Bounding pulse
L-HF
Pulmonary congestion
Hydrostatic pressure
Interstitial pulmonary edema
alveoli
Alveolar pulmonary edema
Dyspnea
Dificulty of feeding
Chest retraction
Breath sound : crackle
Concentric hypertrophy
Peripheral congestion
Hepatomegaly
Pressureoverload
CARDIOLOGY CONGENITAL HEART DISEASESTHEIR STUDY AND TREATMENT 1999b Oliver W. Caminos, M.D.
Normal PDA
Oxygen saturation in the newborn
Pulmonary artery
Pulmonary volume , pressurePulmonary volume , pressure
PreloadPreload
LV hypertrophyLV hypertrophy
CO
O2 not enoughO2 not enough
Blood flow through AortaBlood flow through Aorta
Pulmonary arteryPulmonary artery
BPBP
compensate
Left side HFLeft side HF
+ Baroreceptor+ Baroreceptor
HRcontractility
HRcontractility
+Symp
+ RAAS+ RAAS
P in RV , RAP in RV , RA
VolumeVolume
compensate
RV hypertrophyRV hypertrophy
Right side HFRight side HF
Interfere
arterial elastic
tissue
and induce
endothelial
apoptosis
Heart
failure
(Left
right)
Maternal rubella
in first trimester PDA
Dyspnea
Difficulty feeding
Physical examination and lab investigation
Tachypnea with chest
retraction
Blood flow from
aorta to pulmonary
artery
Pulmonary congestion
Cardiomegaly
Hepatomegaly
Echocardiogram
found 5mm PDA
Bounding pulse of extremities
Hypothesis
Management of PDA
• General principal treatment of Congenital Heart
Disease
• Treatment of PDA
- Medical
- Surgical
Management
Congestive heart failure management
• Elimination of the underlying causes
• Elimination of the precipitating or contributing causes
• Control of heart failure state– General supportive treatment– Drug therapy
Congestive heart failure management
General supportive treatment
• Oxygen (40%-50% ) with humidity
• Salt restriction or diuretics
• Predisposing factors
– Fever
– Anemia
– Infection
Congestive heart failure management
Drug therapy
• Inotropic agents : Digoxin
• Diuretics : Furosemide, Thiazides,
Spironolactone
• Afterload reducing agents :
– Mixed vasodilators : ACEI
Congestive heart failure management
• MOA
inhibits sodium-potassium ATPase
intracellular [Na+]&[Ca2+]
force and velocity of myocardial
systolic contraction
Digoxin
• Decrease in the degree of activation of the
sympathetic nervous system and renin-
angiotensin system (neurohormonal
deactivating effect).
• Slowing of the heart rate and decreased
conduction velocity through the AV node
(vagomimetic effect).
Digoxin
• ADR
– Non-cardiac : anorexia, N/V, diarrhea,
visual disturbance
– Cardiac: prolong PR interval, sinus
bradycardia, supraventricular arrhythmias
Digoxin
Diuretics
• ADR : Electrolyte imbalance
– Hypokalemia (Furosemide,
Thiazides)
Diuretics
Captopril, Enalapril
MOA : Inhibition of ACE results in
decreased plasma
angiotensin II
ADR : Proteinuria, Hypotension, Cough
Angiotensin Converting Enzyme Inhibitors
Management of PDA
• Medication : Preterm infant PDA
• Surgery : Congenital heart
defect
Management of PDA
Treatment of PDA : Medication
NSAIDs
Indomethacin, Ibuprofen
MOA : Inhibits prostaglandin synthesis
( PGE2)
ADR : Peptic ulcer, headache, bleeding
tendency
PDA
Heart Failure
No symptom
Surgery at all age groups
Surgical closure or embolization after 1 year of
age
Treatment of PDA : Surgical
Indication - uncontrol medication heart failure
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Ref.: ตั(าร็าก"มาร็เวช่ศาสัตัร็% เล�ม 1 ภ์าคว!ช่าก"มาร็เวช่ศาสัตัร็% คณะแพทยศาสัตัร็% โร็งพยาบาลร็ามาธิ!บดู+, 2542
REFERENCE
Behrman RE, Kliegman RM : Nelson essential of pediatrics. 3th ed. Philadelphia,
WB saunders. 1998.
กฤษฎี+ ปร็ะภ์าสัะว)ดู . ร็)งสั+ว!นื่!จฉั)ย คณะแพทย%ศาสัตัร็%ศ!ร็!ร็าช่พยาบาล . บร็!ษ)ท ท+ซี+จ+ พร็!�นื่ตั!�ง จ(าก)ดู;
กร็"งเทพฯ , 2546
สัมจ!ตัร็% จาร็"ร็)ตันื่ศ!ร็!ก"ล, มาล)ย ว�องช่าญิช่)ยเล!ศ. ก"มาร็เวช่ศาสัตัร็%ผู้�&ป4วยนื่อก; โร็คร็ะบบหลอดูเล�อดู
และห)วใจ. ช่าญิเม�องการ็พ!มพ%: สังขึ้ลา. 2549.
The Indian Journal of prediatrics, volume 75:number 3, 2008.)
-3Park MK. Pediatric cardiology for practitioners. ed. New York: Mosby Year book; 1 9 9 6 .
Fauci AS., Braunwald E, Kasper DL., Hauser SL., Longo DL., Jameson JL, and Joseph L.
Harrison's Principles of Internal Medicine, 17th Ed
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http:// Emergency Care and Transportation of the Sick and Injured, EMS Field Guide and Journal of Emergency Medical Services.
http://emedicine.medscape.com/article/759542-overview
http://cmbi.bjmu.cn/uptodate/pictures/card_pix/pathop13.gif
http://www.doctordek.com/index.php?Itemid=35&id=57&option=com_content&task=view
http://www.dictionary.webmd.com/terms/dyspnea
http://www.perinatal.nhs.uk/screening/presentations/bts/rubella121201.pdf
REFERENCE