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Cardiology Part 2

Cardiology Part 2

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Published by Krisha_Mae_S_O_3187
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Published by: Krisha_Mae_S_O_3187 on Feb 25, 2010
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05/16/2012

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CONGENITAL HEART DISEASES
REVIEW OF THE FETAL CIRCULATION:a.Foramen ovale permits flow from RA to LA so blood can bypass the useless lungs& go directly to systemic circulation b.Ductus arteriosus is second bypass route, allowing blood in pulmonary arteries totransfer directly to the aorta.c.Fetal right ventricle is hypertrophied since it supplies the lungs & periphery via both the FO & DAd.At birth the lungs expand, pulmonary vascular resistance falls, LA pressure rises,closing the FOe.DA persists for hours to days, however, & is finally shut off due to inhibition of  prostaglandin signals that keep it patentf.As lung perfusion increases & the peripheral bypass tracts shut off, the workloadon the LV increases & the right ventricle workload decreasesg.Eventually over the years, the RV shrinks & the LV hypertrophies
The etiology is usually undetermined.
Chromosomal abnormalities, such as Down syndrome, trisomies, Turner’ssyndrome are often complicated by congenital heart diseasesI.
Atrial Septal Defect
:
Pathophysiology: Greater right than left ventricular distensibilty & low pulmonary vascular resistance result in a left to right shunt at the atrial level, thusincreasing flow across the tricuspid & pulmonary valves. As a result, the rightventricle & pulmonary artery are usually enlarged. There is a patent interatrialseptum
Anatomic changes:a.Patent foramen ovale (clinically insignificant) b.Septum primum: affects the lower part of the atrial septum; if large ir may beassociated w/ deformities of AV valvesc.Septum secundum: defect in the fossa ovalisd.Sinus venosus: affects the upper part of the septum near the entrance of the SVCe.Lutembacher syndrome: ASD with mitral stenosis
Clinical features:
Slow weight gain & frequent respiratory tract infections. The patient develops pulmonary HTN. Can lead also to formation of paradoxical embolism
Assessment findings:
hyperdynamic precordium, right ventricular heave, (+) ejection murmur in the pulmonic area. S2 is widely & constantly split
 
DXtic findings:
CXR: the heart & pulmonary segment is enlarged
ECG: there is right axis deviation
Echo cardiogram: enlarged R ventricle
TX:
Prophylactic AB is given to prevent bacterial endocarditis
Surgical closureII.
Ventricular Septal Defect
:
There is persistent patency of the interventricular septum. This is the mostcommon CHD, accounting for 26% of all CHD. A VSD maybe single or multiple& may be found anywhere along the interventricular septum. It is most commonat the MEMBRANOMUSCULAR portion.
Inflow VSD’s also called endocardial cushion defects is associated with tricuspid& mitral valve abnormalities, & most commonly seen in Down’s syndrome
Pathophysiology:
In small defects the size of the shunt is determined by resistance at the defect;small defect= small shunt. If the defect is large, both the size & direction of theshunt are determined by the relative resistances in the pulmonary & systemiccirculation
As long as the pulmonary vascular resistance is lower than the systemic vascular resistance, the shunt is left to right. If the PulVR> SVR the shunt reverses
Large defects tend to result in pulmonary HTN
The size of the LA & LV are directly proportional to the size of the L-R shunt.RVH occurs only when PulVR increases.
Pulmonary HTN can lead to EISENMENGER REACTION ( pulmonary vascular obstructive disease) & reversal of the shunt (R-L)
Clinical Manifestations:
Maladie de Roger: small VSD, left parasternal thrill with loud holosystolicmurmur at 4
th
left intercostal space, has a benign course
Small defect: no discernable manifestation
Large defects: CHF, growth failure, repeated RTI (1-2 months)
Large defect with increased PulmVR: dyspnea on exertion, chest pain, & cyanosis
Assessment findings:
Murmur at midsternal or lower left sternal border 
Tachypnea, ejection click 
DXtic findings:
 
CXR: large defects: cardiomegaly
ECG: biventricular hypertrophy
TX:
Medical: bacterial endocarditis prophylaxis
Surgical closureIII.
Patent Ductus Arteriosus :
Second most common CHD (10%). The ductus arteriosus connects the pulmonaryartery & descending aorta in the fetus & normally closes shortly after birth.Patency of the ductus is common in VLBW infants
Pathophysiology:
Patency maintained during fetal life by combined effects of low oxygen tension & prostaglandin synthesis
The direction of flow thru a large PDA depends on the relative resistances in thePulmonary & Systemic circuits. As long as the former is lower than the latter a L-R shunt is present. If the PulmVR > SVR, a R-L shunt occurs
The size of the shunt depends on the size of the PDA. If the PDA is largeEisenmenger’s reaction can develop.
Clinical manifestations:
CHF, slow growth, repeated RTI, dyspnea, cyanosis
Assessment findings:
Auscultation: continuous machinery-like murmur heard best at the second leftintercostals space
Bounding pulse
DXtic findings:
CXR: cardiomegaly
LVH on ECG
TX:
Medical: Bacterial endocarditis prophylaxis. INDOMETHACIN is used to close aPDA in a NB
Surgical ligation/ division
IV.Coarctation of Aorta:
 Narrowing of the aorta, usually distal to the origin of the subclavian arteries-extensive development of collateral circulation w/ dilatation of intercostalsarteries.

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