A ventricular septal defect (VSD) is a congenital abnormal opening in the ventricular septum that allows communication of blood between the left and right ventricles. VSDs are caused by embryologic malformations of the ventricular septum. They can occur as an isolated lesion or in combination with other congenital cardiac anomalies. The defect can range from a lesion that might require surgery to a miniscule hole in the muscular septum. Blood flow across the defect is typically left to right and depends on the size of the defect and the pulmonary vascular resistance (PVR).
History of the Procedure
In 1950, Bailey first attempted pulmonary artery banding for the treatment of VSDs. Three years later, he attempted direct suture of a VSD using hypothermia and vena caval occlusion. In 1956, Kirklin reported the first cases of direct-vision intracardiac repair of VSDs using the mechanical pump oxygenator. In 1957, Lillehei demonstrated the feasibility of the transatrial approach to VSD repair using cardiopulmonary bypass.
VSDs rank first in frequency on all lists of cardiac defects. They account for 25-40% of all cardiac malformations at birth. US and international frequencies are identical—approximately 1-2 cases per 1000 live births. Studies have shown that the prevalence of VSDs has increased in the United States during the past 30 years. A twofold increase in the prevalence of VSD was reported by the Centers for Disease Control and Prevention from 1968-1980. The Baltimore-Washington Infant Study (BWIS) reported a twofold increase in the prevalence of VSD from 1981-1989. The BWIS study reported that the increase is primarily attributed to more sensitive detection through echocardiography.
VSDs result from a deficiency of growth or a failure of alignment or fusion of component parts of the ventricular septum. Incomplete closure of the interventricular foramen and failure of the membranous part of the interventricular septum to develop result from failure of tissue to grow from the right side of the fused endocardial cushions and to fuse with the aorticopulmonary septum and muscular part of the interventricular septum.
The increase of alcohol and illicit drug use has been identified as possible risk factors for VSD. The National Center on Birth Defects and Developmental Disabilities, Centers for Disease Control and Prevention produced data that show maternal marijuana use during the preconception period is associated with an increased risk of simple VSD. The study goes on to show an increase in use correlated with an increase in VSD prevalence.
A twofold increase in the risk of VSD associated with maternal cocaine use during pregnancy was found in a study at Boston City Hospital in 1991. The BWIS further reported correlations between membranous isolated VSD and paternal cocaine use. Abnormal blood flow to the heart due to the vasoconstricting effects of cocaine is a postulated reason for these increases.
Finally, alcohol consumption has also been associated with increased VSD. The BWIS found that maternal alcohol consumption was associated with small muscular VSD. No correlation was found with membranous VSDs. A study from Finland further found that alcohol consumption was associated with a 50% increase in VSDs.
Correlations are not detected between the muscular VSDs and maternal use of NSAIDs or acetaminophen. Such correlations were also not detected between maternal fever and VSDs.
The VSD permits a left-to-right shunt to occur at the ventricular level. A left-to-right shunt at the ventricular level has 3 adverse hemodynamic consequences: (1) left ventricular (LV) volume overload, (2) increased pulmonary blood flow, and (3) compromise of systemic cardiac output.
The functional disturbance caused by a VSD depends on the magnitude of the shunt, which is a function of the size of the VSD and the status of the pulmonary vascular bed rather than the location of the VSD. A small VSD with high resistance to flow permits only a small left-to-right shunt. A large interventricular communication allows a large left-to-right shunt only if no pulmonic stenosis or high PVR exists because these factors also determine shunt flow. Quantifying the shunt by the ratio of pulmonary-to-systemic circulation (QP/QS) is useful.
The severity of pulmonary vascular disease correlates to the size of the shunt. In time, as PVR increases, irreversible histologic changes may occur within the pulmonary vascular bed. Untreated, a reversal of the flow occurs, leading to a right-to-left shunt with the development of increasing cyanosis (Eisenmenger complex).
The natural history of VSDs encompasses a wide spectrum, ranging from spontaneous closure to congestive cardiac failure and death in early infancy. The spectrum includes possible development of pulmonary vascular obstruction, right ventricular (RV) outflow tract obstruction, aortic regurgitation, and infective endocarditis.
The clinical picture and functional impairment of VSDs primarily depend on the size of the defect, the status of the pulmonary vasculature, and the degree of shunting, and less on the location of the VSD. Note the following features:
A small VSD usually causes no symptoms.
Respiratory distress and mild tachypnea result from abnormal pulmonary compliance due to mild left-to-right shunting.
Because of compromised systemic output and vasoconstriction, infants with moderately sized VSDs may be pale and are often diaphoretic.
Patients with moderately sized VSDs and decreased pulmonary compliance frequently have a history of 1 or more episodes of pneumonia and/or upper respiratory tract infections.
Infants with a large left-to-right shunt often have congestive heart failure and fail to gain weight.
Patients with VSDs complicated by pulmonary hypertension and reversed shunts (ie, Eisenmenger complex) may present with exertional dyspnea, chest pain, syncope, hemoptysis, cyanosis, clubbing, and polycythemia.
Bacterial endocarditis can develop regardless of the size of the VSD and is related to turbulent blood flow through the defect.
The most common physical finding is a harsh grade IV-VI holosystolic murmur. The murmur is best heard along the left sternal border, is usually louder at the third and fourth intercostal spaces, and is widely transmitted over the precordium. The murmur of VSD does not radiate to the left axilla, as with mitral regurgitation, and does not increase in intensity with inspiration, as with tricuspid regurgitation.
Generally, the smaller the defect, the more turbulent the blood flow through it and the louder the murmur. A grade V-VI murmur may be associated with a very high-velocity flow through only a small, hemodynamically insignificant VSD.
A systolic thrill can commonly be palpated in the region of the murmur along the lower left sternal border. A systolic thrill is less common with large VSDs than with moderate or small defects.
Large defects, with appreciable left-to-right shunts, have wide splitting of the S2, which varies with respiration, and the pulmonic component is accentuated.
When the left-to-right shunt is large, a diastolic, low-pitched flow rumble, suggesting increased flow through the mitral valve, is present. This rumble, which is audible at the lower left sternal border, is often associated with LV S3 gallop.
If pulmonary hypertension develops, the holosystolic murmur diminishes and the thrill disappears. In these patients, the pulmonic component of S2 becomes loud, and an RV lift (indicative of RV hypertrophy) may develop. Cyanosis may become evident, and polycythemia follows. A pulmonary ejection sound may also be noted. The murmur of pulmonary insufficiency can develop (ie, Graham Steell murmur).
Supracristal VSDs in the outlet septum may produce murmurs and thrills more prominent in the first or second left intercostal space with radiation upward.
Patients with a supracristal VSD may develop a diastolic blowing murmur of aortic regurgitation. The holosystolic murmur followed immediately by a blowing diastolic murmur may simulate a continuous murmur.
Patients with VSD are especially at risk for endocarditis, pulmonary infection, ventricular arrhythmias, heart failure, and pulmonary hypertension.
Of patients with congenital VSD, 20% have additional cardiac abnormalities. Most abnormalities were detected at the initial assessment stage; however, aortic prolapse and pulmonary stenosis may also develop subsequently.
Aortic regurgitation may result from the high velocity flow beneath a poorly supported right aortic cusp.
The indications for surgical intervention and its timing may be simple or complex. While many investigators have tried to establish an algorithm for management, the decision to intervene is often a combination of the judgment of pediatric cardiologists and surgeons. The approach must carefully consider the patient's age, symptoms, physiology, and anatomy. Many areas are open to interpretation.
Symptomatic infants with large shunts who cannot be managed medically should undergo closure of the defect.
Surgical repair in patients younger than 6 months is undertaken for control of intractable congestive heart failure, recurrent lower respiratory tract infections, or failure to thrive despite medical treatment.
In children younger than 2 years, prompt surgical repair is indicated if pulmonary hypertension begins to develop before an inoperable predominant right-to-left shunt ensues.
Criteria for surgery in children older than 2 years include presence of symptoms, a QP/QS greater than 2:1, cardiomegaly, or elevated pulmonary artery pressure (PAP).
In adults, surgery is usually recommended if the QP/QS is more than 1.5:1. Once the PVR exceeds 60-70% of systemic vascular resistance and the left-to-right shunt diminishes, closure of the ventricular septal defect (VSD) may no longer be indicated.
Surgery is not indicated in asymptomatic patients with normal findings on chest radiographs and ECGs and a QP/QS of less than 1.5:1.
Patients with subarterial VSD and aortic cusp prolapse, supracristal VSD with aortic regurgitation, or perimembranous VSD with aortic regurgitation are ordinarily referred for surgery to prevent progression of aortic regurgitation.
Even small VSDs should be closed after a single episode of infective endocarditis if the defect remains open once the infection has been cured.
Ventricular septal defects (VSDs) are classified by the position they occupy in the ventricular septum. The septum is divided into 4 components: the membranous septum, the inlet, the trabecular, and the outlet parts of the muscular septum. (The outlet septum is also called the conal or infundibular septum.) Thus, 4 anatomic types of VSDs exist.
Type I defects are also known as subarterial, outlet, or conal defects. These defects comprise 5% of all VSDs and are located in the outlet portions of the left and right ventricles. The superior edge of the VSD is the conjoined annulus of the aortic and pulmonary valves. Because the aortic and pulmonary valves are in fibrous continuity, this type of defect may also be referred to as doubly committed subarterial. (They are also called juxta-arterial, supracristal, subpulmonary, infundibular, or conoseptal defects.) This VSD is associated with prolapse of the unsupported aortic valve cusps and progressive aortic regurgitation.
Type II defects are also called infracristal, subaortic, perimembranous, or paramembranous defects. These defects are the most common type of VSD, comprising 75% of all VSDs. They occur around the membranous septum and the fibrous trigone of the heart and are associated with a muscular defect at a portion of their perimeter. The defect is near the aortic valve, and the annulus of the tricuspid valve contributes to the rim of the defect. Perimembranous defects are divided into 3 major subtypes according to the adjacent portion of the muscular septum: perimembranous inlet, perimembranous trabecular, and perimembranous outlet.
Type III defects (10% of all VSDs), also called atrioventricular (AV) canal, AV septal, or inlet septal defects, are located in the posterior region of the septum beneath the septal leaflet of the tricuspid valve.
Type IV defects (10% of all VSDs), also called muscular defects, have entirely muscular rims. They may be single but are commonly multiple. Muscular defects may be divided into several categories: inlet, trabecular, central, apical, marginal, and outlet (infundibular). Most commonly, multiple defects occur in the apical trabecular septum. In its most severe form, multiple defects of the ventricular septum are sometimes descriptively referred to as Swiss cheese septum.
A pulmonary-to-systemic vascular resistance ratio greater than 0.9:1 or pulmonary arteriolar resistance greater than 12 Wood units is regarded as an absolute contraindication to surgery.
Pulmonary hypertension is not a contraindication to surgery provided the pulmonary-to-systemic vascular resistance is less than 0.75:1. Furthermore, PVR may be described as reactive when it is lowered by higher inspired oxygen content or vasodilators such as nitric oxide. Nonresponders are described as fixed. Patients whose PVR is reactive may benefit more from repair than those whose PVR is fixed.
A PVR of more than 8 Wood units obtained during cardiac catheterization with pulmonary vasodilatation is a contraindication to surgery.
Abu Zubair meriwayatkan dari Jabir bin Abdullah bahwa Nabi Muhammad SAW bersabda:
"Setiap penyakit ada obatnya. Jika obat yang tepat diberikan dengan izin Allah, penyakit itu akan sembuh".
(HR. Muslim, Ahmad dan Hakim).
Jumat, 01 Januari 2010
Diposkan oleh FX di 10.04
The Holy Al-Qur'an (English version)
- Surah 1 - Al Fatiha THE OPENING
- Surah 2 - Al Baqarah THE HEIFER
- Surah 3 - Ali 'Imran - THE FAMILY OF 'IMRAN
- Surah 4 - Al-Nisa' THE WOMEN
- Surah 5 - Al Ma'idah THE REPAST
- Surah 6 - Al An'am THE CATTLE
- Surah 7 - Al A'raf THE HEIGHTS
- Surah 8 - Al Anfal THE SPOILS OF WAR
- Surah 9 - Al Tawbah THE REPENTANCE
- Surah 10 - Yunus JONAH
- Surah 11 - Hud THE PROPHET HUD
- Surah 12 - Yusuf JOSEPH
- Surah 13 - Al Ra'd THE THUNDER
- Surah 14 - Ibrahim ABRAHAM
- Surah 15 - Al Hijr THE ROCKY TRACT
- Surah 16 - Al Nahl BEES
- Surah 17 - Al Isra' THE NIGHT JOURNEY
- Surah 18 - Al Kahf THE CAVE
- Surah 19 - Maryam MARY
- Surah 20 - TA HA
- Surah 21 - Al Anbiya THE PROPHETS
- Surah 22 - Al Hajj THE PILGRIMAGE
- Surah 23 - Al Mu'minun THE BELIEVERS
- Surah 24 - Al Nur THE LIGHT
- Surah 25 - Al Furqan THE CRITERION
- Surah 26 - Al Shu'ara' THE POETS
- Surah 27 - Al Naml THE ANTS
- Surah 28 - Al Qasas THE NARRATIONS
- Surah 29 - Al 'Ankabut THE SPIDER
- Surah 30 - Al Rum THE ROMANS
- Surah 31 - Luqman LUQMAN
- Surah 32 - Al Sajdah THE PROSTRATION
- Surah 33 - Al Ahzab THE CONFEDERATES
- Surah 34 - Saba' SHEBA
- Surah 35 - Fatir THE ORIGINATOR OF CREATION
- Surah 36 - Ya Sin YA SIN
- Surah 37 - Al Saffat THOSE RANGED IN RANKS
- Surah 38 - Sad SAD
- Surah 39 - Al Zumar CROWDS
- Surah 40 - Ghafir FORGIVER
- Surah 41 - Fussilat EXPOUNDED
- Surah 42 - Al Shura CONSULTATION
- Surah 43 - Al Zukhruf THE GOLD ADORNMENTS
- Surah 44 - Al Dukhan THE SMOKE
- Surah 45 - Al Jathiyah THE KNEELING DOWN
- Surah 46 - Al Ahqaf WINDING SAND-TRACTS
- Surah 47 - Muhammad MUHAMMAD
- Surah 48 - Al Fath THE VICTORY
- Surah 49 - Al Hujurat THE CHAMBERS
- Surah 50 - Qaf QAF
- Surah 51 - Al Dhariyat THE WINDS THAT SCATTER
- Surah 52 - Al Tur THE MOUNT
- Surah 53 - Al Najm THE STAR
- Surah 54 - Al Qamar THE MOON
- Surah 55 - Al Rahman THE MOST GRACIOUS
- Surah 56 - Al Waq'iah THE INEVITABLE
- Surah 57 - Al Hadid IRON
- Surah 58 - Al Mujadilah THE WOMAN WHO PLEADS
- Surah 59 - Al Hashr THE MUSTERING
- Surah 60 - Al Mumtahinah THAT WHICH EXAMINES
- Surah 61 - Al Saff THE BATTLE ARRAY
- Surah 62 - Al Jumu'ah FRIDAY
- Surah 63 - Al Munafiqun THE HYPOCRITES
- Surah 64 - Al Taghabun THE MUTUAL LOSS AND GAIN
- Surah 65 - Al Talaq DIVORCE
- Surah 66 - Al Tahrim PROHIBITION
- Surah 67 - Al Mulk THE DOMINION
- Surah 68 - Al Qalam THE PEN
- Surah 69 - Al Haqqah THE SURE REALITY
- Surah 70 - Al Ma'arij THE WAYS OF ASCENT
- Surah 71 - Nuh NOAH
- Surah 72 - Al Jinn THE SPIRITS
- Surah 73 - Al Muzzammil THE ENFOLDED ONE
- Surah 74 - Al Muddaththir THE ONE WRAPPED UP
- Surah 75 - Al Qiyamah THE RESURRECTION
- Surah 76 - Al Insan MAN
- Surah 77 - Al Mursalat THOSE SENT FORTH
- Surah 78 - Al Naba' THE GREAT NEWS
- Surah 79 - Al Nazi'at THOSE WHO TEAR OUT
- Surah 80 - 'Abasa HE FROWNED
- Surah 81 - Al Takwir THE FOLDING UP
- Surah 82 - Al Infitar THE CLEAVING ASUNDER
- Surah 83 - Al Mutaffifin THE DEALERS IN FRAUD
- Surah 84 - Al Inshiqaq THE RENDING ASUNDER
- Surah 85 - Al Buruj THE CONSTELLATIONS
- Surah 86 - Al Tariq THE NIGHT STAR
- Surah 87 - Al A'la THE MOST HIGH
- Surah 88 - Al Ghashiyah THE OVERWHELMING EVENT
- Surah 89 - Al Fajr THE DAWN
- Surah 90 - Al Balad THE CITY
- Surah 91 - Al Shams THE SUN
- Surah 92 - Al Layl THE NIGHT
- Surah 93 - Al Duha THE GLORIOUS MORNING LIGHT
- Surah 94 - Al Sharh THE EXPANSION OF THE BREAST
- Surah 95 - Al Tin THE FIG
- Surah 96 - Al Alaq THE CLINGING CLOT
- Surah 97 - Al Qadr THE NIGHT OF POWER
- Surah 98 - Al Bayyinah THE CLEAR EVIDENCE
- Surah 99 - Al Zalzalah THE EARTHQUAKE
- Surah 100 - Al 'Adiyat THOSE THAT RUN
- Surah 101 - Al Qari'ah THE GREAT CALAMITY
- Surah 102 - Al Takathur THE PILING UP
- Surah 103 - Al 'Asr TIME THROUGH THE AGES
- Surah 104 - Al Humazah THE SCANDALMONGER
- Surah 105 - Al Fil THE ELEPHANT
- Surah 106 - Quraysh THE TRIBE OF QURAYSH
- Surah 107 - Al Ma'un THE NEIGHBOURLY ASSISTANCE
- Surah 108 - Al Kawthar THE ABUNDANCE
- Surah 109 - Al Kafirun THOSE WHO REJECT FAITH
- Surah 110 - Al Nasr THE HELP
- Surah 111 - Al Masad THE PLAITED ROPE
- Surah 112 - Al Ikhlas THE PURITY OF FAITH
- Surah 113 - Al Falaq THE DAYBREAK
- Surah 114 - Al Nas MANKIND
- Acute Coronary Syndromes
- Angina Pectoris
- Anomalous Left Coronary Artery From the Pulmonary Artery
- Aortic Coarctation
- Aortic Dissection
- Aortic Regurgitation
- Aortic Stenosis
- Aortic Stenosis, Subaortic
- Aortic Stenosis, Supravalvar
- Ashman Phenomenon
- Atrial Fibrillation
- Atrial Flutter
- Atrial Myxoma
- Atrial Septal Defect
- Atrial Tachycardia
- Atrioventricular Block
- Atrioventricular Dissociation
- Atrioventricular Nodal Reentry Tachycardia (AVNRT)
- Benign Cardiac Tumors
- Brugada Syndrome
- Complications of Myocardial Infarction
- Coronary Artery Atherosclerosis
- Coronary Artery Vasospasm
- Digitalis Toxicity
- Dissection, Aortic
- Ebstein Anomaly
- Eisenmenger Syndrome
- First-Degree Atrioventricular Block
- HACEK Group Infections (Infective Endocarditis)
- Heart Failure - Decompensatio Cordis
- Holiday Heart Syndrome
- Hypertensive Heart Disease
- Junctional Rhythm
- Loeffler Endocarditis
- Long QT Syndrome
- Lutembacher Syndrome
- Mitral Regurgitation
- Mitral Stenosis
- Mitral Valve Prolapse
- Myocardial Infarction
- Myocardial Rupture
- Paroxysmal Supraventricular Tachycardia
- Patent Ductus Arteriosus
- Patent Foramen Ovale
- Pericardial Effusion
- Pericarditis Acute
- Pericarditis, Constrictive
- Pericarditis, Constrictive-Effusive
- Pulmonic Regurgitation
- Pulmonic Stenosis
- Right Ventricular Infarction
- Saphenous Vein Graft Aneurysms
- Second-Degree Atrioventricular Block
- Sinus of Valsalva Aneurysm
- Sudden Cardiac Death
- Tetralogy of Fallot
- Third-Degree Atrioventricular Block
- Torsade de Pointes
- Tricuspid Regurgitation
- Tricuspid Stenosis
- Unstable Angina
- Ventricular Fibrillation
- Ventricular Septal Defect
- Ventricular Tachycardia
- Wolff-Parkinson-White Syndrome