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Clinical Medicine 3 > Lecture 5 (Peds Cardio)-Exam 2 > Flashcards

Lecture 5 (Peds Cardio)-Exam 2 Flashcards

1
Q

What is congenital heart disease? What is it also known as?

A
  • A malformation of theheart, aorta, or other large blood vessels that change the normal flow of blood through the heart.
  • Also known ascongenital heart defect, congenital heart malformation, congenitalcardiovascular disease, congenital cardiovascular defect, & congenital cardiovascular malformation.
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2
Q

Congenital Heart Disease (CHD)
* Most frequent form of what?
* Born with what?
* Affects how many kids?

A
  • CHD is the most frequent form of major birth defect in newborns.
  • Born with the defect but can present at all ages
  • Affects ~ 8 out of every 1,000 newborns
  • Each year more than 35,000 babies in the US are born with CHD
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3
Q

Congenital Heart Disease (CHD)
* What are the sxs?
* What is the spectrum?

A
  • Signs & symptoms – depend on the type and severity of the defect, can include: asymptomatic, cyanosis, CV collapse, CHF
  • Benign -> Life threatening
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4
Q

Causes of CHD
* What is the mcc?
* Maternal exposures?
* Family history?
* Prematurity?

A
  • Most congenital heart defects have no known cause
  • Maternal Exposures: Medications, Viruses, Diseases
  • Family History: 3 x increased risk when a first-degree relative has CHD
  • Prematurity: 2 to 3x higher in preterm= gestational age <37 weeks
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5
Q

Causes of CHD
* Genetic? (3)

A
  • Genetic syndromes -Chromosome abnormalities (trisomy)
  • Genetic syndromes -Single Gene Mutation (marfan’s)
  • Genetic syndromes -Other: CHARGE syndrome, VACTERL association
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6
Q

Three common classifications of congenital heart disease, according to the American Heart Association.

A
  • Septal defects
  • Obstructive defects
  • Cyanotic defects
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7
Q

What are all the different septal defects?

A
  • Patent Ductus Arteriosus (PDA)
  • Atrial Septal Defect (ASD)
  • Ventricular Septal Defect (VSD)
  • Atrioventricular Canal Defxect (AV canal)
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8
Q

Patent Ductus Arteriosus (PDA)
* Communication between what?
* Shunt?

A
  • Persistent communication between descending thoracic aorta & pulmonary artery
  • Left to right shunting (acyanotic aka no blue blood)
    * Left to right meaning Aortic blood is being shunted into pulmonary artery which leads to increase blood/dilation of left atrium/ventricule

  • Occurs in 3-8 of every 10,000 full-term births,
  • 2:1 female-to-male ratio
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9
Q

What are the risks that can cause PDA?(5)

A
  • Risks: prematurity (~8 in 1,000), perinatal distress, hypoxia, Down syndrome, Rubella in first trimester
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10
Q

PDA clinical manifestations:
* May be what into adulthood?
* What are some common signs in babies?(5)

A
  • May be asymptomatic (into adulthood)
  • Poor feeding and growth
  • Sweating while feeding or crying
  • Fast breathing
  • Rapid pulse
  • Tiring very easily
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11
Q

PDA clinical manifestations:
* What does the exam show?

A
  • Continuous Machinery Murmur (classic sign)
  • Bounding peripheral pulses
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12
Q

PDA-Diagnosis
* What imaging can be done? What are the results?
* What is gold standard?

A
  • CXR- normal; may have cardiomegaly (if severe)
  • ECG – normal; LVH and left atrial abnormality
  • ECHO – Gold Standard test
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13
Q

PDA-Treatment
* What is the treatment?

A
  • Observation (often resolves without intervention)
  • IV Indomethacin (preterm infants-28 weeks)-> CLOSE PDA
  • Surgical intervention if doesn’t close with Indomethacin
    * Surgical ligation <6kg; Percutaneous occlusion >6kg or in adolescents &adults
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14
Q

Atrial Septal Defect (ASD)
* What is it?
* Shunt?
* Difficult to differentiate between what?

A
  • Hole in the septum between the two atria - “hole in the heart”
  • One of the most common etiologies of right heart dilation due to L->R Shunting
  • Difficult to differentiate a PFO from an ASD
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15
Q

Atrial Septal Defect (ASD)
* How many causes of all congenital heart diease?
* Occurs in how many births in the US?

A
  • 10% - 15% of all congenital heart disease
  • Occurs 1-2 in 1,000 live births in the US
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16
Q

What are the risks of ASD?

A

family history, genetic disorders, drugs/alcohol

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17
Q

ASD
* Most common congenital lesion in adults after what?

A

Most common congenital lesion in adults after bicuspid aortic valves (Second most common congenital heart defect in adults)

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18
Q

ASD clinical presentation:
* Small ASD=
* Large ASD=

A
  • Small ASD= no symptoms until adulthood, usually >30 years
  • Large ASD= infants and children symptomatic
    * recurrent respiratory infections, difficulty breathing, tiring when feeding (infants), dyspnea on exertion, fatigue, palpitations, arrhythmias, rarely heart failure

All depends on size of defect

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19
Q

ASD- Clinical Presentation
* Adults manifest what?
* What does the exam show?

A

Adults manifest same symptoms + increased risk of heart failure
* recurrent respiratory infections, difficulty breathing, tiring when feeding (infants), dyspnea on exertion, fatigue, palpitations, arrhythmias, rarely heart failure

Exam-
* Wide fixed split S2, systolic ejection murmur – left upper sternal border
* Right ventricular heave (at LSB)

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20
Q

ASD patho
* How is the blood moving and why?
* What does the moving of blood cause?

A
  • Difference in compliance between the Right Atrium + Right Ventricle as compared to Left Atrium + Left Ventricle + the size of defect = shunting of oxygenated from left side of heart to right side
  • Increased pulmonary blood flow from L->R shunting= increased pulmonary artery pressure = Pulmonary HTN
  • Increased blood flow from L->R shunting= increased volume to R Atria = R Ventricle enlargement
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21
Q

What is the MC place for ASD? What are the other places?

A
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22
Q

ASD diagnosis:
* What are the different tests and results?
* What is the gold standard?

A

CXR – Normal; may have cardiomegaly with increased pulmonary vascularity (dt increase pHTN)

ECG – Normal; Incomplete RBBB
* Crochetage sign – notching of the peak of the R wave

ECHO- Gold standard test

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23
Q

ASD treatmetn:
* What is the treatment?

A
  • Observation-small ASDs typically resolve by age 5
  • Surgical correction for moderate/large ASDs typically > 2 yrs or persistent small ASDs in adults having significant symptoms
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24
Q

What does ASD lead to?

A

RIGHT Heart Dilatation
* This is because right side is more compliant

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24
Q

What is the EKG sign for ASD?

A
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25
Q

Patent Foramen Ovale (PFO)
* What is it?
* Not considered an ASD, why?
* Most important potential manifestation is what?

A
  • Open communication between right and left atria
  • Not considered an ASD because no septal tissue is missing
  • Most important potential manifestation is ischemic stroke due to embolism
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26
Q

Patent Foramen Ovale (PFO)
* Occurs in how many people?
* Often persists into what?
* Most patients are what?

A
  • Occurs in about 25 % of the normal population
  • Often persists into adulthood
  • Most patients are asymptomatic
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27
Q

What septal defect is not considered CHD and why?

A

PFO because only occurs after birth when the foramen ovale fails to close (not techially born with it)

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28
Q

What causes Left heart dilation?

A

VSD and PDA

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29
Q

Ventricular Septal Defect (VSD)
* What is it?
* Most common type of what?
* Occurs in how many people?

A
  • Hole in the septum between the two ventricles
  • Most common type of congenital heart disease in childhood
  • Occurs 4 in 1,000 live births in the US

ASD=ADULTS

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30
Q

What are the risks of VSD?

A

family history, genetic disorders (trimosy 21), a drugs/alcohol

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31
Q

VSD-Clinical presentaion
* Small VSD=
* Large VSD=

A
  • Small VSD= asymptomatic, murmur may be detectable at 4 - 10 daysold, systolic thrill present
  • Large VSD= present at 3-4 weeks of life with symptoms of tachypnea, sweating, poor feeding, poor weight gain, arrhythmias, absent thrill, possible pulmonary HTN and heart failure
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32
Q

What is shown on exam for VSD?

A

harsh/blowing holosystolic murmur heard best at lower left sternal border (smaller = louder)

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33
Q

Pathophysio of VSD
* What is happening is small, moderate and large VSD?

A
  • Small: high resistance to flow permits only a small L-> R shunt, RV pressure remains normal or only minimally elevated
  • Moderate: RV pressure decreases after birth, the L -> R increases, may lead to volume overload of the left atrium and ventricle
  • Large: little resistance to flow, large L-> R shunt = increased pulmonary blood flow ->increased pulmonary venous return-> increased volume load to LV->LV dilation
34
Q

VSD- Diagnosis
* What are the different tests? Results
* What is goal standard?

A
  • CXR –Normal; increased pulmonary vascular markings, left atrial enlargement, LV & RV hypertrophy
  • ECG- Normal; may show LVH in moderate/severe (increased voltage in V5 and V6 or leads II, III)
  • ECHO- Gold Standard test
35
Q

VSD
* What is the treatment?

A

Observation-small VSDs, 75% close by 2 yrs old
* Surgical- moderate/large VSD with heart failure symptoms-patch closures, transcatheter closures

36
Q

Eisenmenger’s Syndrome
* What is it?
* Caused by what?

A
  • Left to right shunt reverses to become RL due to prolonged increased pressure
  • Caused by: VSD, ASD, PDA, AV Canal defect
37
Q

Eisenmenger’s Syndrome
* What are the sxs?
* What are the classic exam findings?
* What is the mean age death?

A
  • Symptoms: cyanosis, pulmonary HTN, syncope, atrial and ventricular arrhythmias, heart failure
  • Classic exam findings: Cyanotic lower extremity, clubbing of nails, SOB at rest, palpitations
  • Mean age death: 37 years old
38
Q

What are the obstructive defects? (3)

A
  • Aortic Stenosis
  • Pulmonary Stenosis
  • Coarctation of the Aorta
39
Q

Coarctation of the aorta:
* What it is?
* How many of the CHD?
* How many births?
* What is the gender predominance?

A
  • Narrowing of the Aorta typically around ductus arteriosus in upper thoracic aorta.
  • 5% of CHD
  • 4 in 10,000 live births in the US
  • 2:1 male predominance
40
Q

Coarctation of the aorta:
* Risks: genetic disorders, familial risk

A

Turners syndrome
-workup for this very common

41
Q

Coarctation of the Aorta-Clinical Manifestations (MILD)
* What happens in neonate, infant/children, adults?

A
  • Neonate= asymptomatic, especially if PDA persistent
  • Infant/Children= chest pain, cold extremities with activity
  • Adults= HTN
42
Q

Coarctation of the Aorta-Clinical Manifestations (MOD/SERVERE)
* What are the sxs?

A

irritability, sweating, poor feeding, poor weight gain, heart failure and SHOCK when PDA closes

43
Q

Coarctation of the Aorta:
* What does the exam show?

A
  • Decreased perfusion/pulses in lower extremities
  • Reduced systolic BP in the lower extremities compared to upper extremities
  • Continuous Systolic murmur – radiates to the back/scapula/chest
44
Q

Coarctation of the Aorta- Diagnosis
* What are the dx tests? What are the results?
* What is gold standard?

A
  • CXR – Cardiomegaly (neonate), Notching appears in ribs due to erosion by the large collateral arteries (children & adults)
  • ECG – Normal; LVH
  • ECHO- Gold Standard Test
45
Q

What is the txt of coarctation of the aorta?

A
  • Maintain the PDA- IV prostaglandin
  • Surgery-balloon angioplasty, stenting
46
Q

What are the acyanotic lesions? What does it result in?

A
  • Patent Ductus Arteriosus (PDA)
  • Atrial Septal Defect (ASD)
  • Ventricular Septal Defect (VSD)
  • Atrioventricular canal (AV canal)
  • Pulmonary stenosis
  • Aortic stenosis
  • Coarctation of the Aorta

Result in pulmonary over-circulation

47
Q

Cyanotic defects:
* What are the 5 Ts?

A
  • Tetralogy of Fallot (TOF)
  • Tricuspid anomalies
  • Truncus arteriosus
  • Total anomalous pulmonary venous return (TAPVR or TAPVC)
  • Transposition of the great arteries (TGA)
48
Q

Cyanotic defects:
* Results from what?

A

Result from mixing of deoxygenated with oxygenated blood or R->L shunting

49
Q

What is the mnemonic cyanotic congenital heart defects?

A
  • One big trunk:Truncus arteriosus
  • Two interchanged vessels: Transposition of the Great Vessels
  • Three:Tricuspid Atresia
  • Four:Tetralogy of Fallot
  • Fivewords:Total Anomalous Pulmonary Venous Return
50
Q

Cyanosis in CHD:
* To be present, how much deoxyhemoglobin must be present?
* What does that equate to on room air?
* What affects level of O2 sat at which cyanosis is detected?

A
  • To be present, 3-5 g/dL of deoxyhemoglobin must be present
  • Equates to O2 sat of 80-85% on room air
  • Total Hgb levels affect level of O2 sat at which cyanosis is detected
51
Q

Cyanosis in CHD:
* What can happen with infants?

A

Infants have high fetal Hbg levels= lower O2 levels before cyanosis visible

52
Q

When may Cyanosis be observed? (4)

A
  • Normal infants have central cyanosis for 5 - 10 minutes after birth as the oxygen saturation rises from 85% to 95% by 10 minutes of age
  • Persistent cyanosis is always abnormal and should be evaluated
  • First few weeks of life
  • Episodically through childhood if uncorrected
53
Q

What is important history of cyanotic CHD?

A
54
Q

Tetralogy of Fallot (TOF)
* Most common what?
* How many live births?
* How many of all CHD?
* WHat are the risks?

A
  • Most common Cyanotic Congenital Heart Disease
  • 4-5 in 10,000 live births in the US
  • 7%-10% of all congenital heart disease
  • Risks: Down’s, DiGeorge Syndrome
55
Q

Tetralogy of Fallot (TOF)
* What are the 4 components?

A
  • Large VSD
  • RV outflow obstruction (Pulmonary Stenosis)
  • Overriding aorta
  • Right ventricular hypertrophy
56
Q

Tetralogy of Fallot (TOF)-Clinical Manifestations
* When do they become symptomatic?

A
  • Typically asymptomatic until 2-5 months of age
57
Q

Tetralogy of Fallot (TOF)-Clinical Manifestations
* What is a tet spell?

A

hypercyanotic & hypoxic episode (increased R ->L shunting)
* acute cyanosis that develops when infant is agitated, feeding and resolves
* toddlers/older children might instinctively squat when they’re short of breath

58
Q

What does the exam show in tetralogy of fallot?

A
  • NO Murmur during Tet Spells
  • Palpable RV impulse
  • Systolic, crescendo-decrescendo murmur at LSB (when calm), Loud S2
59
Q

Tetralogy of Fallot (TOF)
* What are the dx tests? What do they show?
* What is gold standard?

A
  • CXR-Boot shaped heart
  • EKG- RV hypertrophy
  • ECHO-Gold Standard
60
Q

What is the tetralogy of fallot tx?

A
  • Tx-Surgical Repair <6 months old
61
Q

Transposition of the Great Arteries (TGA)
* What is it?
* Most common what?
* How many of CHD?
* How many births?

A
  • Aorta arises from RV & Pulmonary artery from LV
  • Most common cyanotic congenital heart defect in the Newborn
  • 3% of CHD (20% of all cyanotic)
  • 4.7 in every 10,000 live births in the US
62
Q

Transposition of the Great Arteries (TGA)
* What does the exam show?

A
  • cyanosis, tachypnea
  • systolic murmur if VSD, single S2
63
Q

Transposition of the Great Arteries (TGA)
* What is the dx test? What does it show?
* What is the tx?

A
  • CXR- egg-shaped heart (after 1st week), with narrowing of the mediastinum
  • Tx-Surgical Repair (often 1st week of life), administer
    prostaglandin
64
Q

What does this show?

A

Transposition of the Great Arteries (TGA)

65
Q

What does this show?

A

Transposition of the Great Arteries (TGA)

66
Q

Tricuspid Atresia
* What is it?
* What is needed for survival?

A
  • No tricuspid valve = no flow RA->RV->decrease pulmonary blood flow
  • PDA, ASD or VSD are necessary for survival (give prostaglands)
67
Q

Tricuspid atresia:
* How many of CHD?
* How many live births?
* In 25% of the cases great arteries are what?
* What is the mortality rate if untreated?

A
  • 1-2% of CHD
  • 1 in every 10,000 live births in US
  • In 25% of the cases great arteries are transposed with VSD & PS
  • High mortality rate if untreated <10% survival at 1 year old
68
Q

Tricuspid Atresia-Clinical Manifestations
* What are the sx? When do sxs start?

A
  • 50% present with symptoms on the first day of life
  • Tachypnea, cyanosis, poor feeding
69
Q

Tricuspid Atresia-
* What does the exam show?

A
  • Cyanosis at birth, Hepatomegaly (if CHF present)
  • Single S2, Grade 2/6 or 3/6 holosystolic murmur LLSB (if VSD present)
70
Q

What is the txt of Tricuspid Atresia?

A

Tx: IV prostaglandin, Surgical Repair (before 1)

71
Q

Total Anomalous Pulmonary Venous Return
(TAPVR)
* What is it?
* How many of CHD?
* How many live births?
* What is the risk?

A
  • All four pulmonary veins fail to make their normal connection to the left atrium
  • ~1% of CHD
  • 1 in every 10,000 live births in US
  • Risks: Heterotaxy
72
Q

Total Anomalous Pulmonary Venous Return (TAPVR)
* What are the four types?
* What is enlarged?

A

4 types: Supracardiac, Cardiac, Infracardiac, Mixed
* entire oxygenated pulmonary venous return mixes with deoxygenated blood

RA and RV enlargement

73
Q

Total Anomalous Pulmonary Venous Return (TAPVR)
* What does the exam show?

A
  • Cyanosis, CHF in first few weeks of life
  • RV Heave
  • fixed split S2, systolic ejection murmur LSB
  • diastolic rumble across Tricuspid valve
    * if pulmonary obstruction present – cyanosis & loud single S2
74
Q

Total Anomalous Pulmonary Venous Return (TAPVR)
* What is the treatment?

A

Tx- Surgical Repair in infancy

75
Q

Truncus arteriosus:
* What is it?
* How common?
* How many births?
* What is a risk?

A
  • Pulmonary, systemic and coronary circulations originate from single arterial trunk
  • Rare <1% of CHD
  • 6-10 per 10,000 live births in the US
  • Risks: DiGeorge’s syndrome
76
Q

Truncus Arteriosus
* What does the exam show?
* What is the tx?

A
  • Exam-CHF, cyanosis within the first few week of life Single S2, Systolic murmur at LSB
  • Tx- Surgical Repair in infancy
77
Q

Key Physical Exam Components Cyanotic Heart Disease? (9)

A
  • Vitals (Include Pulse ox, BP in upper and lower extremities)
  • Weight and growth
  • Document central or peripheral cyanosis
  • Note location, timing and loudness of murmurs, if present
  • Note gallop or splitting of S2
  • Palpate chest for heaves and thrills
  • Strength and quality of pulses
  • Check for splenomegaly and hepatomegaly
  • Lungs – rales/signs of CHF
78
Q

Diagnosis of Cyanotic Heart Disease
* What is not helpful?
* What can help distinguish heart disease from other causes of cyanosis? What is the issue though with neonates?

A
  • Labs not helpful
  • PaO2 in response to breathing 100% O2 may help distinguish heart disease
    from other causes of cyanosis
    * neonates will not demonstrate this due to fetal Hgb
79
Q

Diagnosis of Cyanotic Heart Disease
* What are the primary tests? What do they show?

A
  • Primary tests – Chest X-ray and ECG
  • CXR may show abnormal position of the aortic arch may be clue to dx of CHD
  • ECG useful in evaluation of chamber size, electrical axis and conduction, right ventricular hypertrophy
80
Q

What is the gold standard of sx cyanotic heart disease?

A
  • Echo-Gold Standard
81
Q

Treatment of Cyanotic CHD
* What does it depend on?
* Obstructive lesions require what?
* What is the process of etralogy of Fallot
* What happens if the neonates tolerate o2 levels in the 70s?

A
  • Depends on age of patient, hemodynamic stability and previous interventions
  • Obstructive lesions require a patent ductus arteriosus – patency may
    require prostaglandins
  • Tetralogy of Fallot -surgically repaired in first 4-12 months of life, others in first few weeks
  • Neonates tolerate oxygen saturation rates in the 70’s – administering oxygen is not always required or recommended and such decisions are made by a specialist
82
Q

What patients need antimicrobial prophylaxis for the prevention of bacterial endocarditis?

A
  • Unrepaired Cyanotic CHD
  • Completely repaired CHD with prosthetic material or device the first six months after the procedure
  • Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device

Clinical Medicine 3 (27 decks)

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