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FETAL CIRCULATION -The fetal circulation is the circulatory system of a human fetus, often encompassing the entire fetoplacenta circulation that also includes the umbilical cord and the blood vessels within theplacenta that carry fetal blood. The fetal circulation works differently from that of born humans, mainly because the lungs are not in use: the fetus obtains oxygen and nutrients from the mother through the placenta and the umbilical cord
CAUSES 1. familial 2. exposure to rubella 3. failure of the heart structure to progress 4. Exposure to teratogens
CLASSIFICATION Formerly, Congenital Heart disorders were classified as: 1. Acyanotic Heart Diseaseinvolves either a stricture to the flow of blood or a shunt that moves blood from the arterial to the venous system (oxygenated to unoxygenated blood, left-toright shunts) 2. Cyanotic Heart Disease
abnormality that permits some of the systemic venous return ( un oxygenated blood) to by pass the lungs and enter general circulation directly. ( right-to-left shunts.)
FOUR CLASSIFICATIONS IDENTIFY DISORDERS WITH: A. Increased pulmonary blood flow B. Obstruction to blood flow leaving the heart C. Mixed blood flow D. Decreased pulmonary blood flow
1. DISORDERS WITH INCREASED PULMONARY BLOOD FLOW -Disorder associated with increased pulmonary blood flow involve blood flow from the left side of the heart to the right side through some abnormal opening or connection between the two systems or the great arteries. TYPES: VSD ASD AVC Defect PDA
VENTRICULAR SEPTAL DEFECTS - abnormal connection between the right and the left ventricles -accounts for about 30% of all instances of congenital heart disease.
PATHOPHYSIOLOGY
*s/s of CHD
CAUSES incomplete looping of the heart during days 24-28 of development. Faults with NKX2.5 gene
DIAGNOSIS 1.X ray - (small ) can be normal ( large ) often show cardiomegaly 2. Cardiac auscultation
Intense murmur reflects the size of the defects 3. Cardiac ultrasound - Non-invasive confirmation of cardiac auscultation 4. Cardiac catheterization - To more accurately measure ventricular pressures.
TREATMENT 1. SMALL no treatment requires MODERATE-LARGE 1ST few months treated medically A. digoxin & diuretics & ACE inhibitor (captopril) B. high caloric formula C. naso gastric feeding D. surgery - with the following indications: 1. Failure of congestive cardiac failure to respond to medications
2. VSD with pulmonic stenosis 3. Large VSD with pulmonary hypertension 4. VSD with aortic regurgitation
ATRIAL SEPTAL DEFECT -abnormal connection between the right and left atria -more common in girls than in boys Blood flow-left to right shunts TYPES: Ostium primum Ostium Secondum
ATRIOVENTRICULAR CANAL DEFECT -also called endocardial cushion defect -Results from incomplete fusion of the endocardial cushion
DIAGNOSIS Chest x ray & echocardiogram TREATMENT Pulmonary artery banding Surgery Anticoagulant and antibiotics
PATENT DUCTUS ARTERIOSUS - direct connection between the main pulmonary artery & aorta -inability of the ductus arteriosus to close until 3 months in the extra utero.
SIGNS & SYMPTOMS SMALL asymptomatic LARGE signs of CHF -wide pulse pressure -presence of continuous machinery murmur in the upper left chest. DIAGNOSIS 1. Echocardiogram 2. chest x ray 3.Presence radial pulse during birth
2. DISORDERS WITH OBSTRUCTION TO BLOOD FLOW LEAVING THE HEART -number of congenital anomalies that cause the blood flow leaving the heart to be obstructed because a vessel or a valve is narrower than usual. - BP before the narrowing, BP after the narrowing -Prohibits enough blood from reaching its intended site TYPES Coarctation of the Aorta Pulmonary Stenosis Aortic Stenosis
COARCTATION OF THE AORTA - there is narrowing along aorta due to a constricting band - Accounts for about 6% in all CHD TYPES a. Preductal coarctation b. Ductal coarctation c. Postductal coarctation
Absent or reduced femoral pulse 2. BP higher in upper extremeties 3. Headache & epistaxis 4. impaired circulation in the lower extremeties 5. myocardial hypertrophy
PULMONARY STENOSIS -there is a narrowing of the pulmonary valve or the pulmonary artery just distal to the valve - due to abnormal development of the fetal heart during the first 8 weeks of pregnancy -10% of all CHD -These problems can include: *A valve that only has one or two leaflets instead of three. *A valve that has leaflets that are partially fused together. *A valve that has thick leaflets that do not open all the way.
AORTIC STENOSIS -Stenosis, or stricture, of the aortic valve prevents blood from passing freely from the left ventricle of the heart into the aorta. 7% of all CHD -may result to pulmonary edema
SIGNS & SYMPTOMS Children-asymptomatic -typical murmur Severe-decreased cardiac output e/b: faint pulse hypotension tachycardia inability to suck for long periods angina DIAGNOSIS ECG
TREATMENT Administer beta-blocker or calcium channel blocker Balloon valvuplasty Artificial Valve Replacement Post-op- anticoagulant, antibiotic
-involve mixing of blood from the pulmonary and systemic circulation in the heart chambers
INCLUDES: Transposition of the Great Arteries Total Anomalous pulmonary venous return Truncus arteriosus Hypoplastic left heart syndrome
-The
aorta arises from the right ventricle instead of the left, and the pulmonary artery arises from the left ventricle instead of the right. Incompatible with life 5% of CHD
SIGNS & SYMPTOMS 1. fatigue 2. dyspnea 3. cyanosis MANAGEMENT 1. provide O2 2.position on fowlers
TOTAL ANOMALOUS PULMONARY VEIN RETURN Pulmonary Veins return to the right atrium or the superior vena cava instead of the left atrium as they normally would. 2% of CHD A patent foramen ovale or an atrial septal defect mustbe present, or else the condition is fatal due to a lack of systemic blood flow.
TRUNCUS ARTERIOSUS -One major artery or trunk arises from the left and right ventricles in place of separate aorta and pulmonary artery vessels
HYPOPLASTIC LEFT HEART SYNDROME -1%-3% OF CHD -left ventricle is non functional - left side of the heart is severely underdeveloped.
TREATMENT -Prostaglandin therapy -Inhalation of combined nitrogen and oxygen -full heart tranplant
4. DISORDERS WITH DECREASED PULMONARY BLOOD FLOW -Involve some type of obstruction to blood flow in the pulmonary artery INCLUDES: Tricuspid atresia Tetralogy of fallot
TRICUSPID ATRESIA -Tricuspid valve is completely closed, allowing no blood to flow from the right atrium to the right ventricle.
CLINICAL MANIFESTATION progressive cyanosis poor feeding tachypnea over the first 2 weeks of life holosystolic murmr due to the VSD left axis deviation on electrocardiography and left ventricular hypertrophy (since it must pump blood to both the pulmonary and systemic systems)
TREATMENT PGE1 to maintain patent ductus arteriosus modified Blalock-Taussig shunt to maintain pulmonary blood flow by placing a Gore-Tex conduit between the subclavian artery and the pulmonary artery. cavopulmonary anastomosis (hemiFontan or bidirectional Glenn) to provide stable pulmonary flow Fontan procedure to redirect inferior vena cava and hepatic vein flow into the pulmonary circulation
TETRALOGY OF FALLOT 4 Defects 1. pulmonary stenosis 2. ventricular septal defect 3. overriding aorta 4. right ventricular hypertrophy
A narrowing of the right ventricular outflow tract and can occur at the pulmonary PULMON valve (valvular stenosis) or just below ARY the pulmonary valve (infundibular stenosis)
STENOSI S
A hole between the two bottom chambers (ventricles) of the heart. The defect is centered around the most superior aspect of the ventricular septum (the outlet septum), and in the majority of cases is single and large
overriding aorta
An aortic valve with biventricular connection, that is, it is situated above the ventricular septal defect and connected to both the right and the left ventricle
The right ventricle is more muscular than normal, causing a characteristic boot-shaped (coeur-en-sabot) appearance
Unoxygenated
blood from the SVC & IV empties into the RA & proceeds to the RV via the tricuspid valve.But because of the pulmonary stenosis, not all unoxygenated blood can pass through the pulmonary artery to be delivered to the lungs for oxygenation.There is pooling of the oxygenated blood in the right ventricle, so that pressure gets higher & higher,
Causing
a shunting of the unoxygenated blood through the opening b/w the R & L ventricle (ventricular septal defect) .There is a R & L shunting of the un oxygenated blood. Since the oarta is just overriding, un oxygenated blood goes through the oarta & delivered to the different parts of the body.In an effort of the RV to push as much unoxygenated blood as possible through stenotic pulmonary artery,it causes RV hypertrophy.
SIGNS & SYMPTOMS 1. cyanosis 2.clubbing of the fingers 3.growth retardation 4.polycethemia 5. boot shaped configuration of heart 6. tachypnea