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Cardiology M2 > 11 19 2014 Congenital heart Defects > Flashcards

11 19 2014 Congenital heart Defects Flashcards

1
Q

Formation of heart tube?

A

mesodermal cells make Endocardial cushions which fuse ventrally to make one heart tube. The heart tube will eventually become the endocardium. splanchnic mesoderm will become the myocardium

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2
Q

What will the endocardial cushions eventually become (specific structures:)

A

membranous intraventricular septum – Atrioventricular canal = tricuspid and mitral orfices

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3
Q

What cells make up the aorticopulmonary septum? What is the function of the aorticopulmonary septum?

A

5th week of gestation, neural crest derived mesenchymal cells proliferate. - 180 degree spiral - Divide truncus arterioles into Atrial cannals: pulmonic artery and aorta

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4
Q

Fetal blood circulation:

A

Umbilical cord Ductus venosus: bypass liver circulation IVC Goes into RA and two paths can be taken: 1. Foramen ovale to LV LV –> ascending aorta: coronary arteries, upper body and brain; descending aorta 2. Mix with blood from superior vena cava –> RV –> Pulmonary Artery –> Ductus Arteriosus —> descending aorta From descending aorta Umbilical vein back to Placenta

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5
Q

What happens after birth in infant circulation?

A
  • Lungs expand and 1. decrease pulmonary resistance via dilation of wall and therefore vessels 2. Vascular resistance in vessels of lungs dilate in response to rich O2 blood supply = Decreases RVP and increases LAP. LAP > RAP and foramen ovale is shut Ductus Arteriosus starts closing due to decrease in prostaglandin and increase O2 saturation
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6
Q

Cyanosis

A

blue-purple coloration of the skin and mucous membranes caused by an elevated blood concentration of deoxygenated Hb. Due to Right –> left shunting in congenital heart defects * bypassing lungs

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7
Q

Atrial Septal Defects anatomical cause:

A

Acyanotic: L–> R shunt Persistent opening in the intratrial septum after birth Direct communication between L. and R. A. Common site: ostium secundum

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8
Q

Physiology of Atrial Septal Defects

A

Oxygenated blood from LA →RA Volume overload of RA and RV. Eisenmenger syndrome may occur with increase RV compliance – if developed closure is contraindicated

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9
Q

Clinical presentations of Atrial Septal Defects

A

Most are asymptomatic (infant) If symptoms occur: dyspnea on exertion, fatigue, recurrent lower respiratory tract infections Adults: decreased stamina, palpitations (atrial tachy due to RA enlargement)

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10
Q

Physical findings on exam for Atrial Septal Defects (ASD)

A

Murmur in childhood/ adolescents (upper left systolic)

* murmur not common because pressure gradients are the same.

Systolic impulse along lower-left sternal border (RV heave)

S2 = widened, fixed pattern

RVH: CXR/ECG/Echocardiography

Catherization: RA O2 saturation >> SVC (usually they are the same)

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11
Q

Treatment for ASD?

A

Closure in early infancy

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12
Q

Anatomy and physiology of a Patent Foramen Ovale (PFO) What is it usually associated with?

A

not a true ASD = persistant opening of foramen ovale (persistence of fetal anatomy) Usually silent because it remains closed due to LAP> RAP HOWEVER it can become significant if RAP>LAP – ex. pulmonary hypertension Paradoxical emoblism: thrombus in systemic vein breaks loos : RA -> LA –> systemic arterial circulation

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13
Q

Ventricular Septum defect ( Anatomy)

A

Abnormal opening in the inter-ventricular septum Membranous *

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14
Q

VSD physiology

A

L→R shut - large shunt: volume overload in RV (not frequently), pulmonary circulation, LA, and LV = chamber dilation—systolic dysfunction can lead to pulm. Vascular disease as early as 2 yrs old. -pulm vas resistance = Eisenmenger syndrome

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15
Q

VSD clinical findings (symptoms)

A

Usually asymptomatic if small. Symptoms of heart failure Infants: tachypnea, poor feeding, failure to thrive, frequent lower respiratory tract infections Cyanosis/hypoxia and dyspnea (Eisenmenger syndrome) endocarditus

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16
Q

Physical findings on exam on VSD:

AND TREATMENT of VSD

A

Harsh holosystolic murmur best heard at left sternal border

*smaller = louder

CXR/ECG = Left sided enlargement

  • R. enlargement when eisenmenger develops
  • cyanosis and loud P2 closure (due to increase in Pul. vascular pressure)

Tx. Surgical or percutaneous closure

17
Q

Anatomy of Patent Ductus Arteriosus (PDA)?

Physiology– including 3 major causes?

A

Vessel that connects the left pulmonary artery to the decending aorta in fetal anatomy remains open.

Composed of smooth muscle (which usually reacts to O2 levels)

L –> R shunt that causes volume overload in pulmonary system, LA, LV and aorta

LV – dilate

* Left side of heart dilates

Desaturated blood to go to lower extremities.

  • Rubella (1st trimester)
  • prematurity
  • born@ high altitued
18
Q

Clinical findings on someone with PDA?

A

Early congestive heart failure, tachycardia, poor feeding, slow growth, recurrent lower respiratory

Moderate size lesion= fatigue, dyspnea, palpitations

Adult: Atrial fibrillation due to LA dilation

Turbulent flow = endocarditis (aka Endoarteritis)

19
Q

Anatomy of Congenital Aortic Stenosis

Physiology?

A

Males> females

BICUSPID AORTIC VALVE

Valvular orifice is significantly narrowed

-eccentric stenotic opening

= increase LV P= LVH due to PRESSURE LOAD

(dilation of aorta)

-bicuspid valve becomes progressively fibrosed and calcified (stenosis)

20
Q

Clinical symptoms of congenital aortic stenosis?

A

Severe –infants: tachycardia, tachypnea, failure to thrive, poor feeding

Older children/adult – asymptomatic

  • But when severe = fatigue, exertion dyspnea, angina pectoris, and syncope
21
Q

Clinical findings for chronic aortic stenosis?

A

Harsh crescendo-decrescendo systolic murmur best heard at base of <3 with radiation to the neck

Bicuspid = murmur is preceded by an ejection click.

Severe disease = paradoxical splitting of S2

CXR/ECG: enlarged heart with dilated aorta; LVH

22
Q

Treatment for Congenital Aortic stenosis?

A

Balloon valvuloplasty in infancy * immediately! but only in severe AS

SURGERY may be needed later.

23
Q

Pulmonic Stenosis:

Anatomy and physiology

A

Congenital fusion of the pulmonic valve commissures

PHysiolgoy:

Impairment of RV outflow = increase in RV pressure

= RVH

24
Q

Clinical symptoms of pulmonic stenosis?

mild vs. severe:

A

Mild/moderate = asymptomatic

Severe = dyspnea, exercise intolerance, decompensation, symptoms of right heart failure

25
Q

Physical findings of pulmonic Stenosis?

  • CXR/ ECG findings?
  • Treatment?
A

Peripheral edema

JVP—prominent A-wave

Palpable liver/ abdominal fullness

RV heave over sternum

Loud late-peaking crescendo-decrescendo systolic ejection murmur heard at upper-left sternal border—associated with a palpable thrill

Widening of S2

Pulmonic valve click decreases with inspiration (push cusps into pulm. Artery= muffle sound

CXR/ECG = RVH ; echocardiogram = increased gradient across Pulm. Valve, elevated Rt. Side pressures, RVH

Tx: balloon valvuloplasty

26
Q

Coartation of Aorta: anatomy and physiology?

A

Preductal or postductal discrete narrowing of aortic lumen.

Usually associated with bicuspid valve

Physiology:

decrease anterograde flow = Increase afterload = increase LVP

= LVH

Dilation of intercostal artiers that bypass site of coarctation

= costal notching

27
Q

Clinical symptoms in people with coartation of aorta:

  • infant and severe
  • less severe–childhood?
  • prognosis in asymtomatic patients?
A

Infants: Severe coartation= differential cyanosis (LE are cyanotic)

Less severe: mild weakness or pain in the LE following exercise (claudication) and detected later in childhood due to HTN.

Asymptomatic = UE hypertension later in life

28
Q

Physical findings from examination of coartation of aorta:

-CXR and echo findings?

A

Femoral pulses are weak/ delayed

Differential BP if UE are still getting enough blood (coartaction is in descending aorta)

CXR—notching on inferior surface of posterior ribs; if severe may see actually constriction of aorta

ECG—LVH

Definitive diagnosis: CT, Doppler Echocardiography, MRI= imaging of aorta

29
Q

Treatment of coarctation of aorta

  • neonates
  • if less severe
A

neonates: prostaglandin infusion to maintain patency

Less severe = elective repair via surgery or percutaneous balloon dilatation

30
Q

Tetralogy of Fallot

Anatomy:

A

Abnormal anterior and cephalad displacement of infundibular portion of intraventricular septum

  1. VSD
  2. subvalvular Pulmonic stenosis
  3. overriding aorta
  4. RVH (due to pulmonic stenosis)
31
Q

Physiology behind tetralogy of Fallot

A

R–> left shunt

increase resistance due to pulmonary stenosis = deoxygenated blood returning from systemic veins (RV) goes to LV to systemic arteries

32
Q

Clinical presentation of Tetralogy of Fallot:

A

Dyspnea on exertion

“Spells” on exertion, feeding, crying (systemic vasodilation increased R –> L shunt)

  • irritability, hypoxia,cyanosis

Squatting makes it better (increases systemic vascular resistance)

33
Q

Physical exam findings in Tetralogy of Fallot

  • CXR
  • ECG
A

Mild cyanosis of lips, mucous membranes, digits

Clubbing of fingers and toes

Palpable heave along left sternal border

S2 is single

Pulmonic Systolic ejection murmur

CXR: “boot shaped heart”

ECG = RVH

34
Q

Treatment of Tetralogy of Fallot?

A

Surgical closure of VSD and enlargement of subpulmonary infundibulum

-replace Pulm Valve as adults

35
Q

Anatomy and physiology behind transposition of Great vessels?

A

Aorta arises from RV; Pulmonary artery arises from LV

-failure of aorticopulmonary septum to spiral in a normal fashion

Physiology:

Systemic and pulmonary circulations are in parallel vs. series

Some blood is necessary to maintain life – patent ductus arteriosis = viable in utero

36
Q

Clinical presentation of baby with transposition of great vessels?

A

Appear blue

Cyanosis is apparent on first day of life and progresses rapidly as ductus arteriosis closes

37
Q

Physical exam presentation and Treatment of Transposition of great vessels

A

Palpation of chest = RV impulses at the lower sternal border

Tx. Exogenous psotaglandins or surgery to maintain PDA open/ balloon catheter

* MEDICAL EMERGENCY

* Atrial switch operation

38
Q

Eisenman syndrome:

Physiology

Clinical findings

Physical exam

Tx:

A

Severe pulmonary vascular obstruction that results from chronic left-right shunting through a congenital cardiac defect

*reversal of original shunt

Clinical findings:

Hypoxemia, exertional dyspnea, fatigue, cyanosis

Physical Exam:

erythrocytosis (production of new blood cells) – try to increase Hb

prominent A-wave in JVP due to increase in R sided pressure.

Loud P2

Treatment:

Dual lung and heart transplant

* once condition develops, correction of original defect is contraindicated

Cardiology M2 (25 decks)

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