Cancer Chemotherapy

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Congenital Heart Diseases:

Congenital Heart Diseases

INTRODUCTION:

INTRODUCTION Usually manifest in childhood, or Unrecognised initially and present in adult life Survival to adult life is possible in most cases Incidence of hemodynamically significant anomalies is about 0.8% of live births

THE FETAL CIRCULATION:

THE FETAL CIRCULATION Minimal blood flow through the lungs From placenta blood reaches RA via IVC & to LA directly via foramen ovale Heart develops as a single tube, folds back on itself, divides into two separate circulations Failure to separate - some forms of ASD and VSD Mal-alignment of great vessels with ventricles – TGA, Tetralogy of Fallot & Truncus arteriosus

Slide 7:

ASD at foramen ovale PDA may fail to close after birth Failed aortic development at aortic isthmus – COA Rubella – PDA, VSD, ASD, PS Exposure to drugs / toxins Alcohol misuse – septal defects SLE – Congenital CHB Genetic / chromosomal abnormalities – Down’s Syndrome, Marfan’s Syndrome,DiGeorge’s Syndrome

PRESENTATION OF CONGENITAL HEART DISEASE THROUGHOUT LIFE:

PRESENTATION OF CONGENITAL HEART DISEASE THROUGHOUT LIFE Birth & neonatal period Cyanosis Heart failure Infancy and childhood Cyanosis Murmur Heart failure Failure to thrive Arrhythmia Adolescence & adulthood Heart failure Hypertension Murmur Late Post surgical sequelae Arrhythmia Cyanosis due to shunt reversal

ATRIAL SEPTAL DEFECT:

ATRIAL SEPTAL DEFECT

AETIOLOGY:

AETIOLOGY MC CHD presenting with symptoms in adults MFR - 1:2 3 types: Ostium secundum (90%) Ostium primum (5%); defect in AVS (associated with cleft MV) Sinus venosus (5%) RV more compliant Blood flows from LA to RA through foramen ovale Progressive dilatation of right heart & PA Later PAH and Shunt reversal

CLINICAL FEATURES:

CLINICAL FEATURES Most are symptom free Often detected at routine examination/ CXR Dyspnoea Respiratory tract infections Cardiac failure Arrhythmias – AF

PHYSICAL FINDINGS:

PHYSICAL FINDINGS 1/3 have systolic thrill Volume overload of RV Wide fixed split S2 wide - delay in RV ejection fixed - the septal defect equalises LA & RA pressures throughout the respiratory cycle S2 split narrowed in PHT Systolic flow murmur over PA In large ASD, MDM (flow murmur) over TA

INVESTIGATIONS:

INVESTIGATIONS X ray chest: Cardiomegaly- dilated RA, RV & PA, pulmonary plethora ECG: Incomplete RBBB RAD in Ostium secundum type LAD in Ostium primum type Echo: RV dilatation and hypertrophy, PA dilatation

MANAGEMENT:

MANAGEMENT Ideal age: 3 – 6 years May close spontaneously up to 2 yrs Indication for surgery: Flow ratio > 1.5 : 1 CI- severe PAH and shunt reversal Cardiac catheterization using implantable closure devices Long term prognosis excellent

VENTRICULAR SEPTAL DEFECT:

VENTRICULAR SEPTAL DEFECT

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Most common congenital heart disease Incidence : 1 in 500 LB. Acquired VSD due to acute MI or trauma Aetiology IVS has a membranous and muscular portion Incomplete septation of the ventricles Flow from LV to RV during systole

CLINICAL FEATURES:

CLINICAL FEATURES Grade IV PSM over 3 rd & 4 th LICS near the sternum Radiates all over the precordium Small defect produces loud murmur (maladie de Roger) Large defect produces softer murmur Elevated RV pressure (immediately after birth/ shunt reversal) Spontaneous closure may occur In infants- may present as CF

CLINICAL FEATURES:

CLINICAL FEATURES CF usually absent in the immediate post-natal period and appears in first 4 to 6 wks Tachypnea Prominent parasternal pulsations Indrawing of lower ribs on inspiration IE very common

INVESTIGATIONS:

INVESTIGATIONS X-Ray:- LV enlargement, Pulmonary plethora ECG:- LVH & RVH with/ without RBBB ECHO:- Dilatation and hypertrophy of RV& LV; helps to assess size of the defect Doppler Echo: Helps to predict small defects likely to close spontaneously

MANAGEMENT:

MANAGEMENT Small VSD – no specific treatment other than endocarditis prophylaxis Cardiac Failure in infancy – Digoxin and diuretics Indication for surgical repair- Persistent failure/ pulmonary to systemic shunt > 1.5:1 Serial ECG and ECHO to avoid Eisenmenger’s Syndrome Fully developed Eisenmenger’s Synd - Heart-Lung transplant

PROGNOSIS:

PROGNOSIS Long term prognosis – very good in congenital VSD except in Eisenmenger’s syndrome Patients with Eisenmenger’s – death in 2 nd or 3 rd decade of life without transplantation Maladie-de-Roger syndrome Small muscular VSD Prominent thrill & loud PSM No hemodynamic changes, Normal ECG Spontaneous closure

TETRALOGY OF FALLOT:

TETRALOGY OF FALLOT

AETIOLOGY:

AETIOLOGY Abnormal development of bulbar septum separating the ascending aorta from PA Incidence – 1 in 2000 LB MC cause for cyanosis after 1 st yr of life 4 components of TOF: VSD PS Overriding of Aorta RVH

PATHOLOGY:

PATHOLOGY RV outflow obstruction – MC is sub valvular (Infundibular) May be valvular/ Supravalvular/ both VSD usually as large as aortic orifice  RV pressure  R to L shunt  Cyanosis

CLINICAL FEATURES:

CLINICAL FEATURES Children usually cyanosed. More common in older children. Relief by squatting Usually absent in neonates as RV pr not  LV pr The subvalvular component of RVOT obstruction is dynamic Sudden increase in cyanosis after feeding or crying, may become apnoeic/ unconscious (fallot’s spells)

CLINICAL FEATURES:

CLINICAL FEATURES Stunted growth, clubbing and polycythemia Cyanosis with a loud ESM in the PA Cyanosis may be absent in mild RVOT obstruction (acyanotic TOF) Complications Marked secondary polycythemia Cerebral abscess Pulmonary TB/ Tuberculoma IE CCF

INVESTIGATIONS:

INVESTIGATIONS ECG:- RVH CXR: Abnormally small pulmonary artery “Boot Shaped Heart” with tilted apex ECHO: Diagnostic. Demonstrates that aorta is not continuous with anterior ventricular septum

MANAGEMENT:

MANAGEMENT Cyanotic spells: squatting, nasal O 2 , Morphine, Propranolol Definitive management – total correction of defect by surgical relief of the PS and closure of VSD Primary surgical correction may be done prior to age 5 & definitive correction at later stage

PROGNOSIS:

PROGNOSIS Prognosis after total correction is good especially if performed in childhood. Follow up needed to identify residual shunting, recurrent pulmonary stenosis and rhythm disorders.

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