Congenital heart diseases

Содержание

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Etiology The causes of congenital heart disease are unknown in 90%

Etiology

The causes of congenital heart disease are unknown in 90% of

cases; they are very likely multifactorial with genetic and environmental inputs.
5% of cases are associated with chromosomal abnormalities
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Etiology Less than 1% of congenital defects are clearly environmental: maternal

Etiology

Less than 1% of congenital defects are clearly environmental:
maternal

rubella in the first trimester
Excessive alcohol consumption
Excessive cigarette smoking
Thalidomide
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Etiology The most critical juncture is embryologic cardiac development in gestational weeks 3- 8.

Etiology

The most critical juncture is embryologic cardiac development in gestational

weeks 3- 8.
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Clinical consequences Children with significant congenital anomalies have: Hemodynamic sequel Failure to thrive Retarded development cyanosis

Clinical consequences

Children with significant congenital anomalies have:
Hemodynamic sequel
Failure to thrive
Retarded development


cyanosis
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Clinical consequences Increased risk of chronic or recurrent illness Infective endocarditis

Clinical consequences

Increased risk of chronic or recurrent illness
Infective endocarditis (due to

abnormal valves or to endocardial injury from jet lesions)
The various congenital anomalies are two types: shunts
obstructions
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Shunts Denotes abnormal communication between heart chambers, between vessels, or between

Shunts

Denotes abnormal communication between heart chambers, between vessels, or between chambers

and vessels. Depending on pressure relationships, blood may be shunted from left to right (more common) or right to left
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Right - to – left shunts Right-to-left shunts (cyanotic congenital heart

Right - to – left shunts

Right-to-left shunts (cyanotic congenital heart

disease) cause cyanosis from the outset as poorly oxygenated blood passes into the systemic circulation. They also permit emboli from venous sources to pass directly into systemic circulation (paradoxic embolism)
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Left – to – right shunts Left-to-right shunts include chronic right

Left – to – right shunts

Left-to-right shunts include chronic right

heart overload with secondary pulmonary hypertension and right ventricle hypertrophy, but eventually right-sided exceeds left-sided pressure and the shunt becomes right to left. Cyanosis appears late.
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Left – to right shunt Once significant irreversible pulmonary hypertension develops,

Left – to right shunt

Once significant irreversible pulmonary hypertension develops, the

structural defects of congenital heart disease are considered irreversible
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Shunts Secondary findings in long-standing cyanotic heart disease include: clubbing of

Shunts

Secondary findings in long-standing cyanotic heart disease include:
clubbing of

the fingers and toes
hypertrophic osteoarthropathy
polycythemia
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Obstructions Typically: coarctation Valvular stenoses or atresias These do not cause cyanosis

Obstructions

Typically:
coarctation
Valvular stenoses
or atresias
These do not cause cyanosis

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Left-to right shunts:late cyanosis Atrial septal defect Ventricular septal defect Patent ductus arteriosus

Left-to right shunts:late cyanosis

Atrial septal defect
Ventricular septal defect
Patent ductus arteriosus

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Atrial Septal Defect (ASD) Definition : a secundum atrial defect is

Atrial Septal Defect (ASD)

Definition : a secundum atrial defect is a

hole in the septum primum (at the site of the foramen secundum) not covered by the septum secundum
Anatomy: the defect is high in the atrial septum, and may vary from dime size to virtual absence of the atrial septum.
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Physiology In the vast majority instances, the shunt across to defect

Physiology

In the vast majority instances, the shunt across to defect is

from the left to right atrium in diastole. The two atria act as a single filling chamber with identical pressures if the hole is at least 1 cm in diameter; the flow in diastole is toward the ventricular chamber, which is thinner walled and more compliant,i.e., RV
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Physiology ASD The pulmonary arterial presser is normal in spite of

Physiology ASD

The pulmonary arterial presser is normal in spite of the

huge flow, owing to the distensibility of the normal pulmonary arterioles. Increased pressure work is a late phenomenon if arteriolar obstruction appears, at which time to shunt becomes bidirectional or even net right-to-left (pulmonary hypertension)
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Diagnosis Patients with secundum atrial defect do not become symptomatic until

Diagnosis

Patients with secundum atrial defect do not become symptomatic until

childhood or adolescence. This phenomenon may explain the late discovery of the malformation.
The symptoms consist principally of failure to thrive, dyspnea, and palpitations
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Physical Examination Patient is usually a tall, thin girl (almost 2:1)

Physical Examination

Patient is usually a tall, thin girl (almost 2:1)
Cyanosis is

rare and almost invariably indicates right ventricular outflow tract obstruction (pulmonary stenosis or pulmonary vascular obstructive disease)
Jugular veins are strongly pulsatile
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Physical examination Left chest prominence Auscultation: the first sound tends to

Physical examination
Left chest prominence
Auscultation: the first sound tends to be loud;
Almost

pathognomonic feature is a widely split second sound with a pulmonary closure of normal intensity, barely moving with respiration
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Auscultation There is a soft ejection murmur at the second left

Auscultation

There is a soft ejection murmur at the second left

interspace (louder if there is associated pulmonary stenosis)
And a low-frequency early diastolic rumble at the lower left sternal border
The sounds, the murmurs, and palpable impulse with left chest prominent all indicate a hyperkinetic circulation
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Electrocardiography (ECG) Right ventricular hypertrophy Severe right ventricular hypertrophy indicates obstruction

Electrocardiography (ECG)

Right ventricular hypertrophy
Severe right ventricular hypertrophy indicates obstruction of the

right ventricular outflow tract
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Radiography The chest film shows mild-to-moderate right ventricular and right atrial

Radiography

The chest film shows mild-to-moderate right ventricular and right atrial

enlargement with pulmonary vascular engorgement and a prominent main pulmonary artery segment.
The sinus venosus defect is characterized by the absence of the right superior vena cava shadow and entrance of the horizontal pulmonary vein into the right upper cardiac shadow
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Echo-Doppler Study The Doppler echocardiogram, particularly in color, gives a good

Echo-Doppler Study

The Doppler echocardiogram, particularly in color, gives a good estimate

of the size and direction of the shunt
A warning note should be sounded here lest a patient be referred for surgery on the basis of a false-positive echocardiogram without supporting data from the physical examination,chest film,and ECG
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Management It has been to close surgically all clinically significant secundum

Management

It has been to close surgically all clinically significant secundum

atrial defects any time on diagnosis
Patients operated on in childhood and early adulthood may look forward to normal lives
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Ventricular Septal Defects (VSD) Definition: an opening in the ventricular septum

Ventricular Septal Defects (VSD)

Definition: an opening in the ventricular septum that

allows communication between the right and left ventricles
Anatomy: the defect are of variable size and may be located in any part of the ventricular septum as single or multiple lesions.
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Anatomy VSD Location of VSD: Muscular (defect in the lower trabecular septum) Perimembranou Subpulmonary

Anatomy VSD

Location of VSD:
Muscular (defect in the lower trabecular septum)
Perimembranou
Subpulmonary

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Physiolodgy VSD A ventricular septal opening allows shunting of left ventricular

Physiolodgy VSD

A ventricular septal opening allows shunting of left ventricular blood

into the right ventricle. The amount of shunting depends on the size of the defect and the relative pulmonary and systemic resistances. A large left-to-right shunt is associated with increased water in the lung, accounting for the symptom of tachypnea.
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Diagnosis A ventricular septal defect is most often detected by the

Diagnosis

A ventricular septal defect is most often detected by the

discovery of a murmur on routine examination. The absence of a murmur at birth, and its appearance a few days later, is characteristic of ventrilar septal defects. By contrast, the murmur of infundibular pulmonary stenosis (which is virtually identical on auscultation) is heard at birth
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Physical Examination An infants with a small ventricular septal defects and

Physical Examination

An infants with a small ventricular septal defects and other

cardiac problems appears normal. There is loud murmur, usually loudest at the lower left sternal border.
The infant with a large ventricular defect is often scrawny, with discordant height and weight, although both measure may be below the fifth percentile.
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Physical Examination Tachypnea as high as 100 breaths/min is common Peripheral

Physical Examination

Tachypnea as high as 100 breaths/min is common
Peripheral pulses are

small
Liver is often enlarged
Cardiac impulse is visibly
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Auscultation Pansystolic murmur Loudest at the lower left sternal border Without

Auscultation

Pansystolic murmur
Loudest at the lower left sternal border
Without treatment, the

heart rate is fast and a gallop rhythm may be present at the apex
The gallop sound is diastole at a fast heart rate may become a mid-diastolic rumble as the heart slows with digoxin therapy
Pulmonary rhonchi and rales are common
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Electrocardiography (ECD) In the patient with a small ventricular septal defect,

Electrocardiography (ECD)

In the patient with a small ventricular septal defect, the

ECD is normal
With increasing larger defects, there is, first, left ventricular hypertrophy, and then, with the largest defects, both ventricular hypertrophy
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Radiography Both the heart size and the pulmonary vasculature are normal

Radiography

Both the heart size and the pulmonary vasculature are normal

in infants with small ventricular defects
With larger defects, the heart is proportionally large, with increased pulmonary vascularity
The left atrial shadow may be large.
Pneumonitis, atelectasis, or aspiration may be evident
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Echo-Doppler Study A Doppler search for additional associated ventricular septal defects

Echo-Doppler Study

A Doppler search for additional associated ventricular septal defects should

be made in all cases.
Differences between right ventricular and left ventricular pressures are recorded and possible pressure gradients between the ight ventricle and pulmonary artery are estimated
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Management Small ventricular defects. The majority of patients with ventricular septal

Management

Small ventricular defects. The majority of patients with ventricular septal

defects are and remain asymptomatic because they defects are small. Only 15% of all patients with a VSD require surgical intervention; even among the symptomatic infants, only 30% come to surgery.
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Management of the Large Ventricular Defect The most common problems are

Management of the Large Ventricular Defect

The most common problems are

congestive heart failure and failure to thrive.
Congestive heart failure is managed initially with digoxin and diuretics, but only rarely is there more than minimal relief of symptoms
Surgical correction is desirable before right heart overload and pulmonary vascular disease develop
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Patent Ductus Arteriosus (PDA) Definition. In the fetus, the ductus arteriosus

Patent Ductus Arteriosus (PDA)

Definition. In the fetus, the ductus arteriosus permits

blood flow between the aorta(distal to the left subclavian artery) and the pulmonary artery
At term, and under the influence of relatively high oxygen tension and reduced local PG synthesis, muscular contraction closes the ductus within 1 to 2 days of life.
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PDA Persistent patency beyond that point is generally permanent. About 85%

PDA

Persistent patency beyond that point is generally permanent.
About 85% to 90%

of PDAs occur as isolated defects. The length and diameter (up to 1 cm) are variable.
There is associated left ventricular hypertrophy and pulmonary artery dilatation
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PDA Although initially asymptomatic, and notable only for a prominent heart

PDA

Although initially asymptomatic, and notable only for a prominent heart

murmur (described as “machinery-like”), long-standing PDA induces pulmonary hypertension with subsequent right ventricular hypertrophy and finally right-to-left shunting to produce late cyanosis
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PDA Early closure of a PDA (either surgically or with prostaglandin

PDA

Early closure of a PDA (either surgically or with prostaglandin administration

in otherwise normal infants) is therefore advocated
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Right-to-left Shunts: Early Cyanosis Tetralogy of Fallot Transposition of the great vessels Truncus arteriosus

Right-to-left Shunts: Early Cyanosis

Tetralogy of Fallot
Transposition of the great vessels
Truncus arteriosus

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Tetralogy of Fallot Ventricular septal defect (VSD) Dextroposed aorta overriding the

Tetralogy of Fallot

Ventricular septal defect (VSD)
Dextroposed aorta overriding the VSD
Pulmonic stenosis

with right ventricular outflow obstruction
Right ventricular hypertrophy
Cyanosis is present from birth or soon after
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Diagnosis Newborns (often) and children (less commonly) may be admitted with

Diagnosis

Newborns (often) and children (less commonly) may be admitted with

evidence of left-side failure, indistinguishable from that seen in patients with large ventricular defect. These patients have only mild pulmonary stenosis at this time
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Diagnosis of tetralogy Fallot Older children and adults with tetralogy of

Diagnosis of tetralogy Fallot

Older children and adults with tetralogy of Fallot

who have not undergone surgical repair almost never show evidence of congestive heart failure unless there are complicating factors (bacterial endocarditis, anemia, aortic regurgitation). They have cyanosis and exercise intolerance of varying degrees; they have moderate or severe pulmonary stenosis.
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Diagnosis of tetralogy Fallot They are cyanotic and have clubbing of

Diagnosis of tetralogy Fallot

They are cyanotic and have clubbing of the

fingers and toes; after running, even walking, they may assume a squatting position
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Diagnosis Hypercyanotic spells occur mostly in infants; these consist of uncontrollable

Diagnosis

Hypercyanotic spells occur mostly in infants; these consist of uncontrollable

crying with increasing cyanosis, tachycardia, tachypnea, leading occasionally to unconsciousness, and sometimes even to a cerebral vascular accident.
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Diagnosis The frightening part of these “spells”is that they may occur

Diagnosis

The frightening part of these “spells”is that they may occur

in otherwise healthy looking, pink infants. The conventional explanation, based on less than unassailable evidence,is that the attacks are due to infundibular spasm. Usually, these attacks occur in the morning and last from several minutes to an hour or more
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Physical Examination Results of the physical examination of patients having tetralogy

Physical Examination

Results of the physical examination of patients having tetralogy with

mild pulmonary stenosis are virtually indistinguishable from those for patients with large ventricular defects. In patients with moderate-to-severe pulmonary stenosis, cyanosis and clubbing dominate the picture.
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Physical Examination A systolic thrill may be palpable at the left

Physical Examination

A systolic thrill may be palpable at the left sternal

border, transmitting to the suprasternal notch, but usually not to the carotids.
On auscultation: is usually an apical click (large aorta), a single loud second sound,and grade IV-VI systolic murmur at the lower left sternal border transmitting well to the suprasternal notch
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Physical Examination No diastolic murmur is heard Minor laboratory tests: Increased

Physical Examination

No diastolic murmur is heard
Minor laboratory tests:
Increased hematocrit (50-75%)

is characteristic of cyanotic heart disease in children and adults.
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Minor laboratory test Severe polycythemia, unusual in infancy, may increase the

Minor laboratory test

Severe polycythemia, unusual in infancy, may increase the viscosity

of the blood to a level that would impede oxygen delivery to tissues; the usual manifestation of this are symptoms of the CNS (dizziness, headaches, blackouts).
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Electrocardiography ECG always shows right ventricular hypertrophy often associated with peaked P waves (P pulmonale)

Electrocardiography
ECG always shows right ventricular hypertrophy often associated with peaked

P waves (P pulmonale)
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Radiography The film in a patient with a right – to-

Radiography

The film in a patient with a right – to-

left shunt shows a normal-sized heart with right ventricular contour (“boot-shaped”, like a Dutch wooden shoe), a large aorta (right aortic arch in 20%), and normal or decreased pulmonary vasculature. The main pulmonary artery segment on the left border of the heart is diminished and may even be concave
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Echo – Doppler Study The echo-Doppler study demonstrates the subaortic ventricular

Echo – Doppler Study

The echo-Doppler study demonstrates the subaortic ventricular

defect and the infundibular stenosis, with establish the morphologic diagnosis of tetralogy of Fallot.
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Cardiac Catheterization Cardiac catheterization with angiography provides the morphologic and physiologic

Cardiac Catheterization

Cardiac catheterization with angiography
provides the morphologic and

physiologic
details and is usually performed prior to
surgical repair.
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Management The treatment for tetralogy of Fallot is surgery. The questions

Management

The treatment for tetralogy of Fallot is surgery. The questions

remaining are the nature and limiting of the operation. There are distinct indications even today for Blalock-Taussig shunts in the treatment of tetralogy of Fallot: a) conus coronary artery, and (b) as an emergency measure for severe hypoxic spells, not manageable by medical means.
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Transposition of Great Arteries Origin of the aorta from the right

Transposition of Great Arteries

Origin of the aorta from the right ventricle

and pulmonary artery from the left ventricle. The patient with transposition of the great arteries has two parallel circulations; blood may recirculate repeatedly through the same side of the heart before returning either to the systemic or the pulmonary capillaries.
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Continuation The unoxygenated systemic venous return passes through the right ventricle

Continuation

The unoxygenated systemic venous return passes through the right ventricle

to the aorta and back to the systemic capillaries. The oxygenated pulmonary venous return passes through the left ventricle and returns to the lungs. It is obvious that the transposed circulation is incompatible with life unless there is communication between the two circuits (VSD, ASD)
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Obstructive congenital anomalies Coarctation of Aorta – is a narrowing or

Obstructive congenital anomalies

Coarctation of Aorta – is a narrowing or constriction

of the aortic isthmus. It is a common, potentially fatal congenital cardiac malformation, clearly progressive through the years. 50% occur as isolated defects, the remainder with multiple other anomalies.
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Coarctation of aorta Clinical manifestations depend on the location and severity

Coarctation of aorta

Clinical manifestations depend on the location and severity of

the constriction. Most occur lust distal to the ductus/ligamentum arteriosus (postductal)
Preductal coarctation manifests early in life and may be rapidly fatal. Survival depends on the ability of the ductus arteriosus to sustain blood flow to the distal aorta and
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Continuation and lower body adequately. Even then, there tends to be

Continuation

and lower body adequately. Even then, there tends to be

lower body cyanosis. This form usually involves a 1-to-5 cm segment of the aortic root and is often associated with fetal RV hypertrophy and early right heart failure.
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Continuation Postductal coarctation is generally asymptomatic unless very severe. It usually

Continuation

Postductal coarctation is generally asymptomatic unless very severe. It usually

leads to upper extremity hypertension but low flow in the lover extremities, causing arterial insufficiency ( claudication, cold sensitivity). Collateral flow around the coarctation generally develops, with intercostal rib notching(noted on X-ray views)
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