Case Ll Real)

Subjective data

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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

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

• Pulmonary etiologies

- Pneumonia

- Pneumothorax

• Cardiovascular etiology - CHF

• Metabolic acidosis

- Drug : Aspirin

Subjective data

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

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

Preterm

• Abnormal breath

• 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.

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;

LINK file record murmur

Listening Areas for Common Pediatric Heart Murmurs

Ref.: http://www.aafp.org/afp/990800ap/558.html

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

Diagnosis & Management :

• Chest X-ray

Echocardiograph

Electrocardiogra

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

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.

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

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

- 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

Endocardial cushion

Chordae tendineae

Papillary muscle

Atrioventricular orifice

- Tissue ย��นื่เขึ้&าไปในื่ช่�องว�างขึ้อง Aorta + Pulmonary artery

Cusp 3 แผู้�นื่ Aortic + Pulmonary semilunar

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

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; .

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

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

hypertrophy

Volume Volume OverloadOverload

hypertrophy

Starling’s law

Contractility

Patent ductus arteriosus

Preload

Compensate

baroreceptor

RAA system

contractility

Bounding pulse

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

O2 not enoughO2 not enough

Blood flow through AortaBlood flow through Aorta

Pulmonary arteryPulmonary artery

compensate

Left side HFLeft side HF

+ Baroreceptor+ Baroreceptor

HRcontractility

+ 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

failure

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

General supportive treatment

• Oxygen (40%-50% ) with humidity

• Salt restriction or diuretics

• Predisposing factors

– Fever

– Anemia

– Infection

Drug therapy

• Inotropic agents : Digoxin

• Diuretics : Furosemide, Thiazides,

Spironolactone

• Afterload reducing agents :

– Mixed vasodilators : ACEI

• 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

Heart Failure

No symptom

Surgery at all age groups

Surgical closure or embolization after 1 year of

Treatment of PDA : Surgical

Indication - uncontrol medication heart failure

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2. ฉั+ดูว)คซี+นื่ป>องก)นื่โร็คห)ดูเยอร็ม)นื่ในื่หญิ!งท+�อย��ในื่ร็ะยะม+บ"ตัร็ไดู& ซี��งไม�เคยเป,นื่โร็คห)ดูเยอร็ม)นื่มาก�อนื่

3. ร็ะหว�างตั)�งคร็ร็ภ์%มาร็ดูาควร็หล+กเล+�ยงการ็ไดู&ร็)บร็)งสั+

4. ในื่คนื่ท+�เป,นื่โร็คทางพ)นื่ธิ"กร็ร็มและม+โร็คห)วใจพ!การ็แตั�ก(าเนื่!ดู ควร็ปร็�กษาแพทย%เก+�ยวก)บอ)ตัร็าเสั+�ยง ซี��งอาจเก!ดูขึ้��นื่ก)บบ"ตัร็คนื่ตั�อๆ ไป

การป'องก�น

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

ภ์าคว!ช่าก"มาร็เวช่ศาสัตัร็% คณะแพทยศาสัตัร็% จ"ฬาลงกร็ณ%มหาว!ทยาล)ย . การ็ซี)กปร็ะว)ตั!และตัร็วจร็�างกายในื่เดูก . กร็"งเทพฯ : บ+ยอนื่ดู% เอนื่เทอร็%ไพร็ซี% 2 5 4 9 .

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

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