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Care of Child with Cardiovascular Disorders

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Care of Child with Cardiovascular Disorders Dr. Manal Kloub Outline CHD CHF Hypoxemia Acyanotic disorders Increased pulmonary flow PDA ASD VSD Cyanotic disorders ... – PowerPoint PPT presentation

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Title: Care of Child with Cardiovascular Disorders


1
Care of Child with Cardiovascular Disorders
  • Dr. Manal Kloub

2
Outline
  • CHD
  • CHF
  • Hypoxemia
  • Acyanotic disorders
  • Increased pulmonary flow
  • PDA
  • ASD
  • VSD
  • Cyanotic disorders
  • Obstructive
  • AS
  • PS
  • COA
  • Decreased pulmonary flow
  • TOF
  • Mixed defects
  • TGV or TGA
  • Hypoplastic heart

3
Heart Anatomy and Physiology
4
Cardiac Conduction
5
First Breath
  • Pulmonary alveoli open up
  • Pressure in pulmonary tissues decreases
  • Blood from the right heart rushes to fill the
    alveolar capillaries
  • Pressure in right side of heart decreases
  • Pressure in left side of heart increases
  • Pressure increases in aorta

6
(No Transcript)
7
Congenital Heart Diseases ?
  • Definition
  • It includes primarily anatomic abnormalities
    present at birth that results in abnormal cardiac
    functions
  • The newborns heart begins to beat at 28 days of
    gestation
  • The heart is completely developed on the 9th week
    of intrauterine life

8
Incidence CHD
  • 4 10/100 live births
  • Major cause of death during 1st year of life
    after prematurity
  • Affect both sexes differently
  • It is more likely to be with other congenital
    anomalies e.g. T.E fistula, Renal agenecies and
    diaphragmatic hernia.

9
Etiology CHD
  • Factors associated with increased incidence
  • Prenatal factors
  • Maternal rubella
  • Radiation
  • Alcoholism
  • age gt40 yrs
  • Insulin dependent diabetes
  • fetal intra uterine cardiac viral disease

10
Etiology CHD
  • Genetic factors although the influence is
    multifactorial there is high risk of CHD in
    children who have
  • a sibling with a heart defect
  • a parent with CHD
  • chromosomal aberration e.g. Downs syndrome
  • Born with other congenital anomalies

11
Altered Hemodynamics
  1. Blood flows from high pressure to area of lower
    pressure and with lower resistance, in response
    to the pumping action of the heart
  2. The higher the pressure gradient the greater the
    rate of flow
  3. The higher the resistance the less the rate of
    flow

12
  1. Normally the pressure in the Rt side is lower
    than the Lt side of the heart
  2. The resistance in the pulmonary circulation and
    vessels entering or leaving these chambers have
    corresponding pressure
  3. So if there is septal defect, blood will flow
    from Lt to Rt known as left to right shunt, and
    no desaturated blood flows directly into the Lt
    side of the heart so it is acyanotic defect

13
Cyanotic defects are due to
  • Change in the pressure causing blood to flow Rt -
    to - Lt Shunt.
  • Due to increased pulmonary flow through the
    pulmonary vascular resistance
  • Or obstruction to the blood flow through the
    pulmonary valve and aorta
  • Or due to mixing of the blood between pulmonary
    and systemic circulation e.g. truncus arteriosus
    (the pulmonary artery and the aorta are one
    single vessel that overrides both ventricles

14
Classification and clinical consequences of
congenital Heart Diseases
  • Depending on the severity of the cardiac defect
    and the altered hemodynamics TWO principal
    clinical consequences can occur
  • 1st Consequence is Congestive Heart Failure
  • 2nd Consequence is Hypoxemia

15
Congestive Heart Failure
  • It is the inability of the heart to pump
    adequate blood to the systemic circulation to
    meet the metabolic demands of the body.
  • It is a symptom caused by cardiac defect not a
    disease in itself, it is due to increased work
    load on normal myocardium

16
Congestive Heart Failure
  • Major manifestation of cardiac disease.
  • Under 1 year of age due to congenital anomaly.
  • Over 1 year with no congenital anomaly may be due
    to acquired heart disease.
  • In children failure of one chamber causes change
    in the opposite chamber

17
Pathophysiology of CHF
  • Two categories
  • Rt sided failure the Rt ventricle is unable to
    pump blood to pulmonary artery resulting in
    increase in the pressure in the Rt atrium and
    systemic venous circulations leading to liver and
    spleen enlargement and occasionally edema.
  • Lt sided failure, the left ventricle is unable to
    pump blood into the systemic circulation leading
    to increased pressure in the Lt atrium and
    pulmonary veins. The lungs become congested
    leading to increased pulmonary pressure and
    pulmonary edema.

18
  • Congestive heart failure leads to
  • cardiac muscles damage
  • decrease the cardiac output
  • decrease the flow of blood to the kidneys
  • increase the reabsorption of Na and water and
    increase blood volume
  • increase systemic congestion
  • Distention in neck veins and peripheral veins
  • Edema and hepatomegaly
  • Forehead sweating due to sympathetic response

19
Clinical S S of CHF
  • Pulmonary Congestion
  • Tachypnea
  • Dyspnea
  • Cyanosis
  • Wheezing
  • Grunting
  • Retractions with flaring nares
  • Cough and hoarseness of voice
  • Cardiac Congestion
  • Tachycardia
  • Cardiomegaly
  • Pale cool extremities
  • Weak peripheral pulses
  • Low blood pressure
  • Gallop Rhythm heart beats

20
Clinical S S of CHF
  • Exercise intolerance
  • Orthopnea
  • Sweating
  • Decreased urine output
  • Weakness
  • Fatigue
  • Restlessness
  • Anorexia
  • Systemic Venous Congestion
  • Weight gain (due to edema)
  • Hepatomegaly
  • Peripheral edema especially periorbital area
  • Ascites
  • Neck vein distension

21
? Therapeutic management
  • Goals
  • Improve cardiac function
  • Remove accumulated fluid and Na
  • Decrease cardiac demands
  • Improve tissue oxygenation and decrease O2
    consumption

22
Interventions
  • Fluid restriction
  • Diuretics Lasix (potassium wasting) or
    Aldactone (potassium sparing)
  • Bed rest
  • Oxygen therapy
  • Small frequent feedings soft nipple with
    supplemental NG for adequate calorie intake
  • Pulse oximeter
  • Sedatives if needed

23
Improving Myocardial efficiency
  • By giving Digitalis glycosides (Lanoxin
    /Digoxin)
  • Increase cardiac output
  • Decrease heart size
  • Decrease venous pressure
  • Decrease edema
  • Regulate heart rate
  • Digoxin increases the force of the myocardial
    contraction.

24
Digoxin Therapy
  • Take an apical pulse with a stethoscope for 1
    full minute before every dose of digoxin. If
    bradycardia is detected.
  • lt 100 beats / min for infant and toddler
  • lt 80 beats in the older child
  • lt 60 beats in the adolescent
  • Nursing alert
  • Call physician before administering the drug

25
Signs of Digoxin Toxicity
  • Extreme Bradycardia
  • Arrhythmia
  • Nausea, vomiting, anorexia
  • Dizziness, headache
  • Weakness and fatigue

26
Supplemental Feeding
Infants with cardiac conditions often
require supplemental feeding to provide
sufficient nutrients for growth.
27
  • Angiotensin-converting enzyme (Captopril/capotin)
  • Inhibit the normal function of rennin angiotensin
    in the kidney and vasodilatation occur, decrease
    pulmonary and systemic vascular resistance which
    decreases B/P and cardiac after load
  • Remove accumulated fluid and Na
  • Diuretics. frusamide (Lasix). Thiazide and
    Spironolactone.
  • Possible restriction of fluids and decrease Na
  • Observe fluid intake and out put and Signs of
    dehydration
  • Potassium supplement, because Diuretics increase
    potassium loss

28
  • Decrease cardiac demand
  • Decrease physical activities, by bed rest,
    observe body temp.
  • Treat any infections
  • Improve breathing semi sitting position and
    sedate irritable children
  • Increase tissue oxygenation and decrease O2
    consumption by applying the mentioned measures
    and giving humidified cool O2

29
2nd Consequence Hypoxemia
  • Referred to arterial O2 tension (or pressure
    PaCo2), that is less than normal can be
    identified by ? SaO2 or ?PaO2
  • Hypoxia
  • Reduction in tissue oxygenation that results from
    ?oxygen saturation and PaO2 which results in
    impaired cellular process
  • Cyanosis
  • Blue discoloration of mucus membrane, skin nail
    beds due to reduced O2 saturation, results from
    the presence of deoxygenated hemoglobin in a
    concentration of 5g/dl of blood or more.

30
  • Cyanosis occurs when O2 saturation is 75 - 85
  • May not reflect arterial hypoxemia because both
    O2 saturation and amount of circulating
    hemoglobin are involved
  • In severe anemia no cyanosis despite severe
    hypoxemia, because hemoglobin level may be too
    low to produce blue color
  • On the contrary, in polycythemia there is
    cyanosis and normal PaO2
  • In Heart defects Hypoxemia and Cyanosis result
    from desaturated venous blood entering the
    systemic circulation

31
Clinical manifestations of Hypoxemia
  • Squatting (rarely seen)
  • Polycythemia (increased number of RBC)
  • Clubbing of the finger
  • Hypercyanotic spells

32
Hypercyanotic spells
  • Hypercyanotic spells
  • Cyanosis
  • Hyperapneia (increased depth of breathing)
  • ?Rt -to-Lt Shunt.
  • Rare lt 2 months of age
  • More common in gt1year of age increase in the
    morning and during feeding, crying and defecation
  • Possible consequences
  • CVA
  • Brain abscess
  • ?Development

33
Congenital Heart Diseases
  • TYPES OF
    DEFECTS and

  • Classification
  • 1st Acyanotic ?
    2nd Cyanotic ?
  • ?Pulmonary Obstruction to
    ?Pulmonary Mixed
  • blood flow blood flow
    flow flow
  • ? ?
    ?
    ?
  • ASD
    Tetralogy TPOGA
  • VSD Coarctation of
    of Fallots Truncus
  • the aorta

    arteriosis.
  • PDA
    Tricuspid Hypoplastic
  • Pulmonic stenosis
    Artesia Lt Heart


  • syndrome

34
Right to Left Shunts
  • Occurs when pressure in the right side of the
    heart is greater than the left side of the heart.
  • Resistance of the lungs in abnormally high
  • Pulmonary artery is restricted
  • Deoxygenated blood from the right side shunts to
    the left side

35
Right to Left Shunt
  • Hole in septum obstructive lesion
  • Deoxygenated blood from the right side of the
    heart shunts to the left side of the heart and
    out into the body.

36
Clinical Manifestations
  • Hypoxemia the result of decreased tissue
    oxygenation.
  • Polycythemia increased red blood cell
    production due to the bodys attempt to
    compensate for the hypoxemia.
  • Increase viscosity of the blood heart has to
    pump harder.

37
Potential Complications
  • Thrombus formation due to sluggish circulation.
  • Brain abscess or stroke due to the un-oxygenated
    blood bypassing the filtering system of the lungs.

38
Left to Right Shunt
  • Pressures on the left side of the heart are
    normally higher than the pressures in the right
    side of the heart. If there is an abnormal
    opening in the septum between the right and left
    sides, blood flows from left to the right.

39
Clinical Manifestations
  • The infant is not cyanotic.
  • Tachycardia due to pushing increased blood
    volume.
  • Cardiomegaly due to increased workload of the
    heart.

40
Clinical Manifestations
  • Dyspnea and pulmonary edema due to the lungs
    receiving blood under high pressure from the
    right ventricle.
  • Increased number of respiratory infections due to
    blood pooling in the the lungs promoting
    bacterial growth.

41
? Acyanotic Defects
  • Lt to Rt shunting through an abnormal opening
    or obstructive lesions leading to decrease blood
    flow to various parts of the body.
  • The most common clinical manifestation is heart
    failure. Some of them may be asymptomatic (ASD,
    VSD, PDA)

42
Patent Ductus Arteriosus
43
Patent Ductus Arteriosus (PDA)
  • The fetal ductus artery connecting the aorta and
    the pulmonary artery fails to close within few
    weeks after birth, so the blood flows from the
    high pressure of the aorta to the lower pressure
    of the pulmonary artery (Lt to Rt shunt
  • Ductus normally closes within hours of birth
  • Connection between the pulmonary artery (low
    pressure) and aorta (high pressure)

44
Patent Ductus Arteriosus
  • Incidence
  • Incidence 10
  • It is most common cardiac anomaly
  • One of the most common benign defects
  • The ratio is 2 ? 1?
  • High risk for pulmonary hypertension

45
Clinical Manifestations PDA
  • Might be asymptomatic
  • Show signs of CHF
  • Machinery - like murmur
  • Widened pulse pressure
  • Bounding pulses resulting from runoff of blood
    from aorta to pulmonary artery
  • Risk of bacterial endocarditis and pulmonary
    vascular obstructive disease in later life from
    chronic excessive pulmonary blood flow

46
Diagnosis tests
  • Diagnosis by
  • Chest x-ray enlarged heart and dilated
    pulmonary artery
  • Echo-cardiogram show the opening between
    pulmonary artery and aorta

47
Treatment PDA
  • Medical management by using Endomethacin
    (Prostaglandin inhibitor) which constricts the
    muscle in the wall of the PDA and promotes
    closure
  • Nonsurgical treatment where coil is placed in the
    open duct and acts like a plug used during
    catheterization procedure
  • Surgical Management via small incision made
    between ribs on left hand side and PDA is ligated
    or tied and cut off
  • Prognosis is good with less than 1 mortality

48
Atrial Septal Defect (ASD)
49
Atrial Septal Defect (ASD)
  • An abnormal opening between atria with a Lt-to-Rt
    Shunt. Blood in left atrium flows into right
    atrium.
  • 10 of defects
  • Reduced blood volume in systemic circulation

50
Clinical Manifestations (ASD)
  • May be asymptomatic
  • May develop CHF
  • Characteristic murmur
  • Pt is at risk for atrial dysrythmia ( may be due
    to atrial enlargement and stretching of
    conduction fibers)
  • At risk for pulmonary vascular obstructive
    disease, and emboli formation later in life due
    to chronic increased pulmonary blood flow
  • If left untreated may lead to pulmonary
    hypertension, congestive heart failure or stroke
    as an adult.

51
Diagnosis (ASD)
  • Heart murmur may be heard in the pulmonary valve
    area because the heart is forcing an unusually
    large amount of blood through a normal sized
    valve.
  • Echocardiogram is the primary method used to
    diagnose the defect it can show the hole and
    its size and any enlargement of the right atrium
    and ventricle in response to the extra work they
    are doing.

52
Treatment (ASD)
  • Nonsurgical treatment might use techniques and
    devices during cardiac catheterization to close
    the opening
  • Surgical treatment using surgical dacron patch
    closure of moderate to large defects.
  • After closure in childhood the heart size will
    return to normal over a period of four to six
    months.
  • No restrictions to physical activity post closure
  • Prognosis very low operative mortality, lt1

53
Ventricular Septal Defect (VSD)
54
Ventricular Septal Defect (VSD)
  • It is an abnormal opening between right and left
    ventricles, may vary in size small pinhole to
    the absence of the septum, resulting in common
    ventricle. Frequently associated with other
    defects
  • Lt to Rt Shunt
  • 30 of defects
  • May be classified according to defect location

55
Ventricular Septal Defect (VSD)
  • Small holes generally are asymptomatic
  • Medium to moderate holes will cause problems when
    the pressure in the right side of the heart
    decreases and blood will start to flow to the
    path of least resistance (from the left ventricle
    through the VSD to the right ventricle and into
    the lungs)
  • May be associated with other defects such as (PS,
    TGV,PDA)
  • Many VSD closes spontaneously 1st year of life

56
Clinical Manifestations VSD
  • May develop CHF
  • Characteristic murmur
  • Right ventricular hypertrophy
  • Deficient systemic blood flow
  • High risk of bacterial endocarditis and pulmonary
    vascular obstruction disease
  • May develop Eisenmenger syndrome
  • refers to the combination of systemic-to-pulmonary
    communication, pulmonary vascular disease and
    cyanosis

57
Diagnostic tests VSD
  • Diagnosis heart murmur clinical pearl a
    louder murmur may indicate a smaller hole due to
    the force that is needed for the blood to get
    through the hole.
  • Electrocardiogram to see if there is a strain
    on the heart
  • Chest x-ray size of heart
  • Echocardiogram shows size of the hole and size
    of heart chambers

58
Management VSD
  • Palliative placing band on pulmonary artery to
    decrease pulmonary blood flow
  • Complete repair small defects are reparied with
    purse-string. Large defect require knitted Dacron
    patch sewn over the opening.
  • Post operative complication include conduction
    system disturbances
  • Nonsurgical treatment closure during cardiac
    catheterization are still under study
  • Prognosis risk depend on location of the defect,
    number of defects and other cardiac factors.
    Mortality rate ranges from 5 to 20

59
Surgical Repair
  • Over a period of years the vessels in the lungs
    will develop thicker walls the pressure in the
    lungs will increase and pulmonary vascular
    disease
  • If pressure in the lungs becomes too high the
    un-oxygenated blood will cross over to the left
    side of the heart and un-oxygenated blood will
    enter the circulatory system.
  • If the large VSD is repaired these changes will
    not occur.

60
Medical Treatment VSD
  • CHF diuretics of help get rid of extra fluid in
    the lungs
  • Digoxin if additional force needed to squeeze the
    heart
  • FTT or failure to grow may need higher calorie
    concentration
  • Will need prophylactic antibiotics before dental
    procedures if defect is not repaired

61
? Major Cyanotic Defects
  • Cyanotic defects result from
  • Obstructive defects (PS, AS, COA)
  • And Mixing of desaturated blue venus blood with
    fully saturated red arterial blood within the
    chambers of the heart (TOF, TGV / TGA,
    Hypoplastic heart)

62
Pulmonary stenosis
63
Pulmonary Stenosis (PS)
  • It is narrowing at the entrance of the pulmonary
    artery (pulmonary valve) leads to narrowing and
    obstruction between the right ventricle and the
    pulmonary artery.
  • Resistance to blood flow cause Hypertrophy of
    right ventricle
  • Thickened tissue become less pliable and
    increases the obstruction
  • Right ventricle must work harder to eject blood
    into the pulmonary artery.
  • 7 of defect

64
Clinical Manifestations (PS)
  • Some might be asymptomatic
  • Some might have mild cyanosis or CHF
  • Newborns with severe narrowing will be cyanotic
  • Characteristic murmur
  • Cardiomegally is evident in chest X-ray
  • ? Risk of Bacterial Endocarditis with progressive
    narrowing lead to increase symptoms

65
Diagnostics PS
  • Diagnosis heart murmur is heard clicking sound
    when the thickened valve snaps to an open
    position.
  • Chest x-ray, enlarged heart
  • Electrocardiogram would be normal
  • Echocardiogram most important non-invasive test
    to detect and evaluate pulmonary stenosis
  • Cardiac Catheterization to measure pressures
    and measure the stenosis

66
Management PS
  • Surgical correction
  • Infants Transventricular valvotomy Bock
    procedure
  • Children Valvotomy with cardiopulmonary bypass
  • Nonsurgical treatment
  • Cardiac catheterization to dilate the valve and
    open up the obstruction by using a balloon
    angioplasty
  • Prognosis less than 2 mortality

67
Aortic stenosis
68
Aortic Stenosis (AS)
  • Narrowing of aortic valve causing resistance to
    blood flow in the Lt ventricle, decrease cardiac
    output, Lt ventricular hypertrophy and pulmonary
    vascular congestion.
  • Causes obstruction to blood flow between the left
    ventricle and aorta.
  • Most common form is obstruction of the valve
    itself

69
Aortic Stenosis
  • 6 of defects, 30 incidence of sudden death
  • Aortic valve has two rather than three leaflets.
    Leaflets are thickened or fused.
  • When the aortic valve does not open properly the
    left ventricle must work harder to eject blood
    into the aorta.
  • Left ventricular muscle becomes hypertrophied.

70
Clinical Manifestations (AS)
  • Infants with severe defects
  • Signs of decreased cardiac output and faint
    pulses
  • Hypotension and tachycardia
  • Poor feeding
  • Exercise intolerance
  • Chest pain and dizziness
  • Characteristic murmur
  • Risk for endocarditis, ventricular dysfunction,
    and coronary insufficiency

71
Diagnostics AS
  • Heart murmur of turbulent like noise caused by
    ejection of blood through the obstructed valve.
  • Electrocardiogram is usually normal
  • Echocardiogram will show the obstruction and rule
    out other heart anomalies
  • Exercise stress test provides information on
    impact of the stenosis on heart function

72
Management AS
  • Surgical correction
  • - valvotomy if the closed procedure does not
    work often done when patient is older when
    severe calcium deposits further obstruct the
    valve.
  • Nonsurgical correction
  • - Dilating narrowed valve with balloon
    angioplasty in the cath lab
  • Prognosis
  • Newborn critical conditions mortality 10 - 20
  • Older children elective valvotomy has lower risk
  • Complication Recurrent valve obstruction is a
    complication and if valve replacement is done too
    early the child may outgrow the valve.
    Prophylactic antibiotic needed

73
Coarctation of the Aorta (COA)
74
Coarctation of Aorta (COA)
  • There is localized narrowing near the insertion
    of ductus arteriosus resulting in
  • Increased pressure in proximal structures to the
    defect (Head and upper extremities)
  • Decreased pressure distal to obstruction
  • (body and lower extremities)
  • Congenital narrowing of the descending aorta
  • 7 of defects
  • 80 have aortic-valve anomalies
  • Difference in BP in arms and legs (severe
    obstruction)

75
Clinical manifestations (COA)
  • High B/P and bounding pulses in arms
  • Weak or absent femoral pulses
  • Cool lower extremities with low B/P
  • Signs of CHF in infants
  • Older children may experience dizziness,
    headaches, fainting and epistaxis due to
    hypertension
  • Risk of hypertension, ruptured aorta, aortic
    aneurism or stroke

76
Diagnostics COA
  • In 50 the narrowing is not severe enough to
    cause symptoms in the first days of life.
  • When the PDA closes a higher resistance develops
    and heart failure can develop.
  • Pulses in the groin and leg will be diminished
  • Echocardiogram will show the defect in the aorta

77
Management COA
  • Surgical correction Resection of narrowed
    portion and end - to - end anastomosis or graft
    replacement via thoracotomy incision
  • Nonsurgical treatment balloon angioplasty may be
    successful in some cases but risk of aneurysm
    formation is present
  • Prognosis less than 5 mortality rate in
    isolated coarctation
  • - high risk in infants with other complex
    cardiac defects

78
  • Medical Treatment
  • Prostaglandin may given to keep the PDA open to
    reduce the pressure changes
  • Antibiotic prophylactic need due to possible
    aortic valve abnormalities.
  • Complications
  • Surgical complications kidney damage due to
    clamping off of blood flow during surgery
  • High blood pressure post surgery may need to be
    on antihypertensives

79
Tetralogy of Fallot (TOF)
80
Tetralogy of Fallot (TOF)
  • 6 of defects
  • Most common cardiac malformation responsible for
    cyanosis in a child over 1 year

81
TOF
  • Four Components
  • Ventricular Septal defect - VSD
  • Pulmonary stenosis narrowing of pulmonary valve
  • Overriding of the aorta aortic valve is
    enlarged and appears to arise from both the left
    and right ventricles instead of the left
    ventricle
  • Hypertrophy of right ventricle thickening of
    the muscular walls because of the right ventricle
    pumping at high pressure

82
Clinical Manifestations TOF
  • Dependent on degree of right ventricular outflow
    obstruction.
  • Some infants are acutely cyanosed at birth,
    others have mild cyanosis that progresses over
    the 1st year as the pulmonary stenosis worsen
  • Children are at risk of developing emboli, C.V
    disease, brain abscess, Seizures and loss of
    consciousness, or sudden death following an
    anoxic spell.

83
Clinical Manifestations TOF
  • Acute episodes of cyanosis and hypoxia (blue
    spells) usually during crying or after feeding
  • With increased cyanosis increased clubbing of
    fingers, Squatting, Poor growth
  • Severe irritability due to low oxygen levels
  • tet spells - treated by flexing knees forward
    and upward

84
Knee-chest Position
Nurse puts infant in knee-chest position.
Child with a cyanotic heart defect squats
(assumes a knee-chest position) to
relieve cyanotic spells. Some times called
tet spells.
85
Diagnostic tests TOF
  • Cyanosis
  • Oxygen will have little effect on the cyanosis
  • Loud heart murmur
  • Echocardiogram demonstrates the four defects
    characteristic of tetralogy

86
Management (TOF)
  • Palliative to increase blood flow back to the
    pulmonary artery from right or left subclavian
    artery by doing modified blalock taussig shunt
  • If oxygen levels are extremely low prostaglandins
    may be administered IV to keep the PDA open
  • Prognosis less than 5 total operative mortality
    rate

87
Surgical Treatment
  • Corrective Elective reparit in 1st year of life
    based on increased symptoms.
  • Correction includes
  • Closure of the VSD with dacron patch
  • The narrowed pulmonary valve is dilated
  • Coronary arteries will be repaired
  • Hypertrophy of right heart should remodel within
    a few months when pressure in right side is
    reduced

88
Long Term Outcomes
  • Leaky pulmonary valve that can lead to pulmonary
    insufficiency
  • Arrhythmias after surgery
  • Heart block occasionally a pacemaker is
    necessary
  • Periodic echocardiogram and exercise stress test
    or Holter evaluation

89
Transposition of Great Vessels
90
Transposition of Great Arteries
91
Transposition of Great Arteries or Vessels (TGA
or TGV)
  • Pulmonary artery leaves the Lt ventricle
  • Aorta exits from the Rt ventricle
  • With no communication between systemic and
    pulmonary circulation
  • Males are affected more than females
  • Associated defects such as Septal defects or
    patent ductus arteriosus permits blood to enter
    the systemic circulation and or pulmonary
    circulation for mixing of saturated and
    nonsaturated blood

92
Clinical manifestations TGV/TGA
  • It depends on the type and size of the associated
    defects.
  • If minimum communication present, then children
    are severely cyanosed
  • If PDA or septal defect is present, less cyanosis
    symptoms present but might show signs of CHF.
  • Heart sounds vary according to defects
  • Cardiomegally occur after few weeks of life

93
Management TGV/TGA
  • Surgical Palliative treatment (To provide
    intracardiac mixing)
  • Administration of IV prostaglandin E1 to keep the
    ductus arteriosus open to temporary increase in
    blood mixing and provide O2 saturation of 75 or
    to maintain cardiac output.
  • Rashkin procedure Enlarge septal defect
  • Complete repair
  • Switching the great vessels to their correct
    anatomic position.
  • Prognosis Operative mortality about 5 10

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ACUTE RHEUMATIC FEVER
  • Acute rheumatic fever (ARF) is a systemic disease
    characterized by inflammatory lesions of
    connective tissue and endothelial tissue.
  • It is a primary type of acquired heart disease.

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Etiology/Incidence
  • The pathogenesis is thought to be an autoimmune
    response to group A beta-hemolytic
    Streptococcus.
  • Most attacks of ARF are preceded by an untreated
    streptococcal infection of the throat or upper
    respiratory tract at an interval of 2 to 6 weeks.
  • ARF is not caused by direct infection of the
    organism.
  • ARF is commonly seen in children 5 to 15 years of
    age, during winter months, and in poorer living
    conditions.
  • Incidence is greater in underdeveloped countries,
    although it is on the rise in the United States.

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Altered Physiology
  • There is cross-reactivity between cardiac tissue
    antigens and streptococcal cell wall components.
  • The Streptococcus may no longer be present, but
    auto antibodies attack one's heart (myocardium,
    pericardium, or valves)
  • The unique pathologic lesion of rheumatic fever
    is the Aschoff body, a collection of
    reticuloendothelial cells surrounding a necrotic
    center on some structure of the heart.
  • The inflammatory process involves the heart,
    joints, skin, and central nervous system.

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  • The inflammation may involve the leaflets or
    chordae tendinae of the heart valves, most
    frequently THE MITRAL or aortic valves, resulting
    in sclerosis and fusion of valve margins
  • Valvular incompetence results
  • There is a high recurrence rate.
  • Of those with ARF, 75 progress to rheumatic
    heart disease in adulthood.
  • ARF is a preventable condition with penicillin
    treatment of the primary infection. Erythromycin
    is treatment for those with penicillin
    sensitivities.

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Complications
  • ? Significant chronic heart failure
  • ? Pericarditis, pericardial effusions
  • ? Aortic/Mitral valve regurgitation
  • ? Permanent cardiac damage

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Major Manifestations
  • CARDITIS manifested by significant murmurs,
    signs of Pericarditis, cardiac enlargement, or
    CHF
  • POLYARTHRITIS almost always migratory and is
    manifested by
  • swelling,
  • heat,
  • redness and tenderness
  • or by pain and limitation of motion of two or
    more joints.
  • (The synovial fluid is sterile (

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Cont. Major Manifestations
  1. Chorea, a CNS disorder that lasts 1 to 3 months
    purposeless, involuntary, rapid movements often
    are associated with muscle weakness, involuntary
    facial grimaces, speech disturbances, and
    emotional liability

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Cont. Major Manifestations
  • Erythema marginatum are temporary
    nonpruritic,pink rash.
  • The erythematus areas have pale centers
  • and round or wavy margins, vary greatly in size,
    And occur mainly on the trunk and extremities.
  • Erythema is transient, migrates from place to
    place, and may be brought out by the application
    of heat.
  • (Erythema marginatum)

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Cont. Major Manifestations
  • 5. Subcutaneous nodules are firm, painless
    nodules seen or felt over the extensor surface of
    certain joints, particularly elbows, knees, and
    wrists, in the occipital region, or over the
    spinous processes of the thoracic and lumbar
    vertebrae the skin overlying them moves freely
    and is not inflamed.
  • (Subcutaneous nodule)

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Minor Manifestations
  • History of previous rheumatic fever or evidence
    of preexisting rheumatic heart disease
  • Arthralgiapain in one or more joints without
    evidence of inflammation, tenderness to touch, or
    limitation of motion
  • Fevertemperature in excess of 38C
  • Elevated erythrocyte sedimentation rate (ESR)
  • Positive C-reactive protein (CRP)
  • ECG changesmainly PR interval prolongation

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  • Supporting Evidence of Streptococcal
    Infection
  • Increased titer of streptococcal antibodies
    (Antistreptolysin O or ASO titer)
  • Positive throat culture for group A
    beta-hemolytic streptococci or recent scarlet
    fever

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Treatment
  • Treatment of streptococcal infectiongenerally
    intramuscular (IM) penicillin G (Penicillin L-A)
    erythromycin for patients with penicillin allergy
  • Prevention of permanent cardiac damage
    corticosteroids for patients with Carditis
  • Palliative management of other
    symptomsSalicylates prescribed for patients with
    arthritis (but not while on high-dose
    corticosteroids due to risk of gastrointestinal
    bleeding) antipyretics after diagnosis has been
    established
  • Prevention of recurrences of ARF

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