HEART FORMATION CON’T Weeks 5-8 SVC, IVC form Right and Left Atrium divide Ventricles start to form Aorta and pulmonary arteries Weeks 8-12 Ventricles and mitral and tricuspid valves Aorta and pulmonary artery, aortic arch Week 12:Fetal Circulation begins
TRANSITION FROM THE FETALCIRCULATION Pulmonary vascular resistance falls Ductus venosus and ductus arteriosus close Right-to-left shunting through foramen ovale ceases Timing of these events determines the timing of presentation of congenital heart defects
CYANOTIC HEART DISEASE Cyanotic heart disease is a heart defect, present at birth (congenital), that results in low blood oxygen levels. There may be more than one defect.
CYANOSIS IN CHILDREN Central cyanosis: Cyanosis of the tongue,mucous membranes and peripheral skin, it is necessary to have >3g/dl of reduced Hb to have it. Peripheral cyanosis: It is visible only in the skin of the extremities with normal arterial saturation due to vasomotor instability,ex. cold environment.
CAUSES OF CENTRAL CYANOSISB) LUNG DISEASE D) CNS DEPRESSIONa) RDS a) IVHb) Pneumonia b) Perinatal asphyxiac) Pneumothorax c) Heavy maternal sedationd) Pleural effusione) Diaphragmatic herniaf) T.E.FistulaC) PERSISTENT PULMONARY E) MISCELLANOUS HYPERTENSION a) shock & sepsis b) Hypoglycemia c) Methemoglobinemia d) Neuromuscular conditions ( Werdnig – Hoffman)
RADIOLOGICAL FEATURES CXR may exclude non cardiac causes of cyanosis e.g. RDS. . Meconium aspiration, Diaphgramatic hernia, Pneumothorax Pulmonary Vascular Markings Decreased Increased Heart Size Heart Size Normal Increased Increased( “Boot shaped”) (“ Wall-to-Wall”) TOF Ebstein (“ egg-on-end”) D-TGA Aortic Arch Mediastinum Abdominal Situs
AUSCULTATIONHEART SOUNDS: S1 is normally accentuated in newborns S2 split is normally heard as a slurring rather than a distinct split. S2 is single in many cyanotic lesions especially in, D-TGA, TOF. S2 is widely split in TAPVR, Critical PS.
MURMURS SYSTOLIC EJECTION MURMURS May be heard in the first hours of life. Usually due to ventricular obstruction e.g. AS., PS., TOF DIASTOLIC MURMURS: Rarely heard in newborns Early diastolic murmurs heard in Truncus arteriosus , TOF with absent pulmonary valve Continuous: Continuous murmurs are caused by AV fistulas (not PDA) ABSENT: Silent hearts often characteristic of Tricuspid atresia , Pulmonary atresia & D-TGA.
Examination of CVS in the newborn1.Look for cyanosis and dysmorphology
TETRALOGY OF FALLOT (TOF) Named by Etienne-Louis Arthur Fallot in 1888 Approximately 10% of all complex CHD Single developmental error of the terminal portion of the spiral truncoconal septum Four distinct components: subpulmonic stenosis, VSD, overriding aorta, and RV hypertrophy Often accompanied by other anomalies
DEFINITION Tetralogy of Fallot is the result of unequal division of the conus. Four alterations result: Narrower right ventricle outflow region Defect in the interventricular septum An aorta that overrides directly above the septal defect The right ventricular wall hypertrophies.
FOUR MALFORMATIONS IN TOF A.Pulmonic stenosis B.Overriding aorta C.Ventricular septal defect (VSD) D.Right ventricular hypertrophy
CAUSES Unknown Methylene tetrahydrofolate reductase gene (Portugal study) Maternal rubella during pregnancy Down syndrome CATCH 22(cardiac defects, thymic hypoplasia,cleft palate, hypocalcemia) Right ventricular out flow tract obstruction Deletion of chromosome band 22q11
SIGNS AND SYMPTOMSCyanosis-blue color to the skin, which gets worse when the baby is upset
CONT…………..Failure to gain weightPoor developmentDifficulty in feeding
PATHOPHYSIOLOGY Pulmonary stenosisA narrowing of the right ventricular outflow tract and occur at the pulmonary valve (valvular stenosis) or just below the pulmonary valve (infundibular stenosis). Caused by overgrowth of the heart muscle wall (hypertrophy of the septo parietal trabeculae). These events finally leads to overriding of aorta.
OVERRIDING OF 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 degree to which the aorta is attached to the right ventricle is referred to as its degree of "override."
The aortic root can be displaced toward the front (anteriorly) or directly above the septal defect, but it is always abnormally located to the right of the root of the pulmonary artery.
VENTRICULAR SEPTAL DEFECT 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. In some cases thickening of the septum (septal hypertrophy) can narrow the margins of the defect.[
RIGHT VENTRICULAR HYPERTROPHY The right ventricle is more muscular than normal, causing a characteristic boot- shaped (coeur-en-sabot) appearance as seen by chest X-ray. Due to the misarrangement of the external ventricular septum, the right ventricular wall increases in size to deal with the increased obstruction to the right outflow tract. This feature is now generally agreed to be a secondary anomaly, as the level of hypertrophy generally increases with age.
ADDITIONAL ANAMOLIES stenosis of the left pulmonary artery, 40% of patients a bicuspid pulmonary valve, 40% of patients right-sided aortic arch, 25% of patients coronary artery anomalies, 10% of patients a foramen ovale or atrial septal defect, in which case the syndrome is sometimes called a pentalogy of Fallot, atrioventricular septal defectpartially or totally anomalous pulmonary venous returnforked ribs and scoliosis.
DIAGNOSIS OF TETRALOGY OF FALLOT History –cyanosis,feeding Physical examination: Single accent. S2 ESM CXR: boot shaped heart (coeur en sabot) ECG: RVH Hematocrit-elevated ABG and Oximetry
CYANOTIC OR TET SPELLAnxietyOver sweating (hyperventilation)Sudden increase in cyanosis
CYANOTIC SPELLSSpasm of decrease SVR cryingRVOT Increase R…..L shuntingIncrease systemic venous return DecreaseO2 Increase CO2 Decrease pH Tachypneea
CYANOTIC SPELLS Increase systemic vascular resistance Squat/Knee chest position Ketamine 1-2mg/kg IV Neosynephrine 0.02mg/kg IV Tachycardia Propranolol 0.1mg/ Kg IV Release of infundibular spasm Irritability Morphine 0.2mg/ Kg S.C or IM Hypoxia Oxygen Dehydration Volume Acidosis NaHco3 1mEq/ Kg IV
TOF MANAGEMENT Medical : Correct iron deficiency anemia Correct polycythemia B-Blocker Analgesics-to reduce the ventilatory drive. eg:morphine sulfate Alpha-adrenergic agonists-to improve hemodynamic status by improving the myocardial contractility and increasing heart rate resulting in increased cardiac output. eg:phenylephrine
FACTORS THAT INCREASE THE RISK FORSURGERY Low birth weight Pulmonary artery atresia Major associated anomalies Multiple previous surgeries Absent pulmonary valve syndrome Young or old age Severe annular hypoplasia Small pulmonary arteries High peak RV–to–left ventricular pressure ratio Multiple VSDs Coexisting cardiac anomalies
CONTRAINDICATIONS FOR SURGERY The presence of an anomalous coronary artery Very low birth weight Small pulmonary arteries Multiple VSDs Multiple coexisting intracardiac malformations
POTTS SHUNT A side to side anastomosis of pulmonary artery with aorta is created The Potts shunt has been abandoned because of a tendency toward increased pulmonary blood flow and increasing difficulty with takedown at the time of corrective surgery.
It consists of constructing a shunt between the ascending aorta and right pulmonary artery The Waterston shunt is sometimes used, but it also increases pulmonary artery blood flow. This shunt is more related to pulmonary artery stenosis, which generally requires reconstruction.
SURGICAL MANAGEMENT Surgical: Palliative = Blalock-Taussig shunt for small PA’s Definitive= Total correction
GOAL OF PALLIATIVE SURGERY The goals of palliation for tetralogy of Fallot (TOF) are to increase pulmonary blood flow independent of ductal patency and to allow pulmonary artery growth and even total correction.
ADVANTAGES OF MODIFIEDB-T SHUNT preservation of the subclavian artery, suitability for use on either side, good relief of cyanosis, easier control and closure at time of primary repair, excellent patency rate, and decreased incidence of iatrogenic pulmonary/systemic artery trauma.
CORRECTIVE SURGERY Primary correction is the ideal operation for treatment of tetralogy of Fallot (TOF) and is usually performed under cardiopulmonary bypass (CPB). The aims of the surgery are to close the ventricular septal defect (VSD), resect the area of infundibular stenosis, and relieve the right ventricular (RV) outflow tract obstruction (RVOTO).
CORRECTIVE SURGERY Before cardiopulmonary bypass is initiated, previously placed systemic-to- pulmonary artery shunts are isolated and taken down. Patients then undergo cardiopulmonary bypass. Associated anomalies, such as atrial septal defect (ASD) or patent foramen ovale, are closed.
SURGICAL COMPLICATIONS Early postoperative complications following repair of tetralogy of Fallot (TOF) include the creation of heart block and residual ventricular septal defects (VSDs). Ventricular arrhythmias are more common and are reportedly the most frequent cause of late postoperative death. Sudden death from ventricular arrhythmias has been reported in 0.5% of individuals within 10 years of repair.
TRANSPOSITION OF GREAT VESSELS The hallmark of tranposition of great arteries is ventriculoarterial discordance, in which the aorta arises from the morphologic right ventricle and pulmonary artery arises from the morphologic left ventricle
TRANSPOSITION OF THE GREAT ARTERIES (TGA) Complete TGA or D-TGA Embryological inversion of the great arteries Ventriculoarterial discordance Congenitally corrected TGA or L-TGA Embryological inversion of the ventricles Atrioventricular & ventriculoarterial discordance (double discordance)
CAUSESUnknownAbnormal persistence of the subaorticconus with resorption or underdevelopment of the subpulmonaryconus(infundibulum)
DIAGNOSIS OF TGA Transposition of the great arteries with intact ventricular septum: Prominent and progressive cyanosis within the first 24 hours of life is the usual finding in infants. Transposition of the great arteries with large ventricular septal defect: Infants may not initially manifest symptoms of heart disease, although mild cyanosis (particularly when crying) is often noted. Signs of congestive heart failure (tachypnea, tachycardia, diaphoresis, and failure to gain weight) may become evident over the first 3-6 weeks as pulmonary blood flow increases.
CONTD… Transposition of the great arteries with ventricular septal defect and left ventricular outflow tract obstruction: Infants often present with extreme cyanosis at birth,
SURGICAL REPAIR Balloon atrial septostomy Developed by Rashkind (1965) Enlarges the atrial communication Atrial switch Performed first by Senning (1958) and later modified by Mustard (1964) Atrial baffle is created to direct venous return to the contralateral ventricle
SURGICAL REPAIR Arterial switch Performed first by Jatene (1976) Great arteries transected and reattached to appropriate AV valve Coronary ostia also transplanted Surgical treatment of choice Excellent outcomes so far
Atrial Switch There are two types of atrial switch operations - the MUSTARD operation, and the SENNING operation. Both are similar in principle, but differ in technique. The atrial switch operation is an open heart procedure and is carried out with the assistance of a heart-lung machine. The right atrium is opened, and the wall between the atria is fully removed.
AtrialSwitch Using pericardium (Mustard) or flaps created from the atrial septum and wall (Senning), a "baffle" is constructed directing blood from the veins in the right atrium towards the left ventricle. The same baffle also directs blood from pulmonary veins to the right ventricle. The circulation is therefore restored to normal in a functional sense.
Definitive Procedures Rastelli procedure. Pulmo artery transected distal to its valve and proximal end is oversewn. Rt. Ventricle incised high along its outflow tract. Intraventricular dacron prosthetic tunnel is created between the edge of septal defect and aortic orifice.
EBSTEIN’S ANAMOLY Congenital defect Origins of septal or posterior leaflets, or both, are displaced downward into RV Leaflets are variably deformed Atrialization of right ventricle Anterior leaflet is enlarged and sail-like
EBSTEIN’S ANOMALY The tricuspid valve is abnormal and inserts well down into the RV. There is often severe trisuspid regurgitation, which can lead to death in the fetus or infant. Usually also with ASD so right-to-left flow results in cyanosis.
Physical ExaminationCyanosis and clubbing - Varying degrees ofcyanosis at various times in life and transientworsening with arrhythmiasPrecordial asymmetry-Usually left parasternalprominence and occasionally right parasternalprominence Absent left parasternal ( ie , rightventricular) lift an important negative signJugular venous pulse May be normal Large aand v waves late in the course of the disease,with development of right heart failure
Arterial pulses Usually normal Diminished volumeHeart sounds First heart sound widely split with loud tricuspid component Mitral component may be soft or absent in the presence of prolonged PR interval. Second heart sound usually is normal widely split when the pulmonary component is delayed due to RBBB.
ADDITIONAL HEART SOUNDS AND MURMURS Third and fourth heart sounds commonly present, even in the absence of congestive heart failure (CHF). Summation of third and fourth heart sounds, especially with prolonged PR interval, can mimic an early diastolic murmur. The holosystolic murmur of tricuspid regurgitation at the lower left parasternal area and sometimes at the apex murmur intensity and duration increase during inspiration.
Chest X-Ray: Normal findings Cardiomegaly ( Rounded or Box- like contour ) Small aortic root and main pulmonary artery shadow Decreased pulmonary vasculature Large right atrium
12-LEAD EKG: Rhythm -Usually normal sinus findings Intermittently SVT, paroxysmal SVT, atrial flutter, atrial fibrillation, ventricular tachycardia Abnormal P waves consistent with right atrial enlargement PR interval -Most commonly prolonged May be normal or short in patients with WPW (B) syndrome QRS complex -RBBB Low voltage in many patients
ECG from a patient with Ebsteinsanomaly showing huge P waves andlow amplitude QRS waves. RBBB and Twave inversion are not present on thisECG.
Echocardiogram:Echocardiogram standard for diagnosis.M-mode Paradoxical septal motion Dilated right ventricle Delayed closure of tricuspid valve leaflets more than 65 milliseconds after mitral valve closure
CONTD… Two-dimensional Apical displacement of the septal leaflet of greater than 8 mm/m 2 – Abnormalities in morphology and septal attachment of the septal and anterior tricuspid leaflets Eccentric leaflet coaptation Dilated right atrium Dilated right ventricle with decreased contractile performance Various left heart structural abnormalities
ASSESSMENT OF SEVERITY AND SURGICAL OPTIONS BY ECHOCARDIOGRAPHY Functional right ventricular area less than 35% of total right ventricular area or an atrialized to functional right ventricular ratio greater than 0.5 associated with unfavorable prognosis Functional right ventricular size Degree of septal leaflet displacement Amount of leaflet tethering
CONTD… Magnitude of leaflet deformity and dysplasia Aneurysmal dilatation of right ventricular outflow tract (right ventricular outflow tract-to-aortic root ratio of >2:1 on parasternal short axis view) Moderate-to-severe tricuspid regurgitation
Cardiac Catheterization:Cardiac Catheterization Rarely performed today Confirms echocardiographic findings Can reveal right ventricular electrical activity on the intracardiac ECG with simultaneous right atrial pressure and waveform when the catheter is withdrawn from the right ventricle, back across the tricuspid valve into the right atrium
MEDICAL MANAGEMENT Antibiotic prophylaxis for infective endocarditis Medical therapy for heart failure - Angiotensin- converting enzyme (ACE) inhibitors, diuretics, and digoxin Arrhythmia treatment - Medical treatments such as anti-arrhythmic drugs or radiofrequency ablation of the accessory pathways Curative therapy of SVT with radiofrequency ablation is currently the treatment of choice. The success rate is lower than that in patients without significant structural heart disease.
Factors associated with lower likelihood of success include the following: Accessory pathways located along the atrialized right ventricle Multiple accessory pathways Complex geometry of the pathways Abnormal morphology of the endocardial action potentials in this region
Indications for surgery are generally as follows: New York Heart Association (NYHA) class I-II heart failure with worsening symptoms or with a cardiothoracic ratio of 0.65 or greater NYHA class III-IV heart failure History of paradoxical embolism Significant cyanosis with arterial O2 saturation of 80% or less and/or polycythemia with hemoglobin of 16 g/dL or more Arrhythmias refractory to medical and radiofrequency ablation
SURGICAL MANAGEMENT Approaches: Approaches Tricuspid valve repair is preferred over valve replacement Bioprosthetic valves are preferred over mechanical prosthetic valves. The atrialized portion of the right ventricle can be resected surgically, and the markedly dilated, thin- walled right atrium can be resected. Associated septal defects may be closed
Repair of TV & Closure of ASD: Repair of TV & Closure of ASD Usual preparation for operation & anaesthesia CPB Two venous cannulae Assess atrialized portion for paradoxical movement Body temperature about 25 o C RA incised parallel to AV groove
Palliative procedures include creation of atrial septal defect, closure of tricuspid valve with plication of the right atrium, and maintenance of pulmonary blood flow through aortopulmonary shunt.
TAPVRDefinition -No direct communication exists between the pulmonary veins and the LA. -Instead, they drain anomalously into the systemic venous tributaries or into the RA. Epidemiology -1% of all congenital heart defects. -There is a marked male preponderance for the infracardiac type (male/female ratio of 4:1)
TOTALLY ANOMALOUS PULMONARYVENOUS DRAINAGE(INFRADIAPHRAGMATIC) Allfour pulmonary veins drain to the right side. Below the diaphragm they are always obstructed. Infant presents in first days with cyanosis, circulatory and respiratory failure and collapse.
Pathophysiology1)Mixing of oxygenated and deoxygenated blood before or at the level of the right atrium (total mixing lesion). -Cyanosis -Right atrial blood either passes into the right ventricle and pulmonary artery or passes through an atrial septal defect (ASD) or patent foramen ovale into the left atrium. -Enlarged RA,RV, PA, small or normal LA, LV2) Obstructed pulmonary venous return -severe pulmonary congestion,pulmonary hypertension, hypoxia3) Restriction of PFO or ASD: -diminished LV preload->low cardiac output, small left side heart
CLINICAL MANIFESTATION1)Severe obstruction to pulmonary venous return, -In neonatal period: Cyanosis and severe tachypnea are prominent, but murmurs may not be present. -Severely ill and fail to respond to mechanical ventilation.2)Mild or moderate obstruction to pulmonary venous return and a large left-to-right shunt. - Heart failure in early life - Pulmonary artery hypertension->severely ill. - Systolic murmurs :the left sternal border, gallop rhythm -Cyanosis: mild.3)No pulmonary venous obstruction -No pulmonary hypertension these patients -less likely to be severely symptomatic during infancy. -Clinical cyanosis: mild.
In most cases without obstruction :the heart is enlarged, the pulmonary artery and right ventricle are prominent, and pulmonary vascularity is increased. In neonates with marked pulmonary venous obstruction :a perihilar pattern of pulmonary edema and a small heart
ECHOCARDIOGRAPHY: ESSENTIAL FOR DIAGNOSISA large right ventricle :the pattern of abnormal pulmonary venous connections.A vessel in the abdomen with Doppler venous flow away from the heart is pathognomonic of TAPVR belowthe diaphragm.Shunting occurs almost exclusively from right to left at the atrial level
TREATMENT Medical1.Intensive anticongestive measures with digitalis and diuretics ->in patient without pulmonary venous obstruction2.Metabolic acidosis should be corrected3.In infants with severe pulmonary edema(in infracardiac type and other type) ->ventilator support with oxygen and positive end-expiratory pressure4.PGE1; In patient with PHT (controversial), ->PGE1:increase systemic flow by keeping ductus open. ->In the infacardiac type, PGE1->maintaining the ductus venosus open5.If the size of the interatrial communication appears small and immediate surgery is not indicated ->balloon atrial septostomy or blade septostomy may be performed
NATURAL HISTORY1.CHF occurs in both types of TAPVR with growth retardation and repeated pneumonias2.Without surgical repair, two thirds of the infants without obstruction die before reaching 1 years of age.(d/t superimposed pneumonia)3.Patients with infracardiac type rarely survive for longer than a few weeks without surgery. Most die before 2months of age.
Types of tricuspid atresia Type 1 Type2 Type 3• The • The • The great great great arteries arteries arteries are are d- are l- related transpos transpos normally ed ed
Diagnosis of Tricuspidatresia History Physical examination Investigations
CyanosisGrowth retardationNasal flaringMuscle retraction*Brain abscess and bacterial endocarditis- headache, seizures and neurologic deficit
Cyanosis P Digital clubbing JVP distension H Y Peripheral pulses Apical impulse displaced First heart sound increased S Second heart sound –split Continuous cardiac murmur- I 80%cases C A L examination
INVESTIGATIONS Lab studies- Chest X-rayCBP-polycythemia Cardiomegaly,right atrial enlargement Echo ECG Tall T waves-atrialPresence of ASD enlargement,first degree AV block
CARDIAC CATHETERIZATIONStastusof ductus arteriosusASD if present ATRIAL SEPTOSTOMY
Infants with Infants with decreased increased Palliative pulmonary blood flow pulmonary procedures blood flow Severe Severe Surgicalhypoxemia- congestive proceduresprostagland heart in E failure- digitalis and diuretic therapy
SURGICAL CARE Blalock-Taussig ShuntDefinition: A subclavian artery to pulmonary artery anastamosis.Advantages: Predictability of flow, shunt may grow with the child, post-op congestive heart failure is less common than with other procedures, graft thrombosis is uncommon.
Disadvantages: Inadequate flow is possible, stenosis of the anastomosis is possible due to increased tension on the vessel, possible injury to the phrenic nerve, pulmonary hypertension is possible, small diameter of the subclavian may result in worsened hypoximia. Uses: Tetralogy of Fallot - can restore partial blood flow in the obstruction of the pulmonary circulation. Tricuspid Atresia - improves oxygenation of the desaturated blood due to the the shunt to the pulmonary circulation. Pulmonary Atresia - creates a shunt between systemic and pulmonary circulations
GLENN PROCEDURE Definition: Advantages: A superior vena cava Pulmonary hypertension (SVC) to pulmonary is rare (blood is being artery anastomosis. shunted under low This is an end to side venous pressure), does anastomosis where the not increase the volume right pulmonary artery of work on the heart is divided at the distal (amount of blood end and is attached to returned to the heart is the side of the SVC. unchanged).
GLENN PROCEDUREDisadvantages: Uses: Cyanosis may increase by Used to bypass the right the decreased perfusion to heart, therefore bothlungs, may call for a second palliative procedure becomes useful in such as Blalock-Taussig. anomalies where right Polycythemia secondary to side obstruction occurs, hypoximia may increase such as tricuspid atresia blood viscosity and or tricuspid stenosis. decrease flow through the pulmonary vascular bed thus decreasing oxygen saturations. Shunt is only effective if the child weighs over 8 kg.
FONTAN OPERATION The right atrium is connected to the pulmonary artery directly. Used when it is not possible to have a two ventricle repair (this case has tricuspid atresia). Pulmonary vascular resistance must be low. It is done at age 4 years or so.
TYPE A IAAThe arch interruption occurs distal to the origin of the left subclavian artery.
TYPE B IAAThe interruption occursdistal to the origin of the left common carotid artery.
TYPE C IAAThe interruption occursproximal to the origin ofthe left common carotid artery
PATHOPHYSIOLOGY With an interrupted aortic arch, venous blood returning to the heart goes to the lungs and returns to the left side of the heart as oxygenated blood, so it can go to the body through the aorta. However, oxygenated blood leaving the left ventricle to the Aorta, only goes to vessels proximal to the interruption. These vessels usually go to the upper body and the head.
CONTD… Arteries that come off the Aorta distal to the obstruction get deoxygenated blood from the right ventricle. This blood gets to the descending Aorta through a PDA. Repair of this lesion entails connecting the ascending and descending Aorta and ligating the PDA.
RASTELLI OPERATION An example of a repair of complex CHD with two ventricles. This one had a big VSD, TGA and PS. The severe sub- pulmonary stenosis precluded an arterial switch (it would become the neo-aortic valve), so a conduit joins RV to PA, and the VSD is patched.
SEVERAL PARAMETERS SHOULD BE METTO ENSURE A SUCCESSFUL OUTCOME. The candidate should be aged 4 years or older. A right atrium of normal volume and normal caval drainage should be present. Sinus rhythm should be present. Mean pulmonary artery pressure should be low (ie, < 15 mm Hg), as should mean pulmonary arteriolar resistance. The pulmonary artery-to-aorta diameter ratio should be greater than 0.75.
Nursing management ofclient with cyanotic heart disease
Helping family memebers to adjust Proiding pre operative care Preoperative assessmentNursing Preoprative teaching care Providing post oprative care Post operative assessment and management
NURSING DIAGNOSISImpaired gas exchange R/T altered pulmonary blood flowAltered cardiac output R/T specific anatomic defectActivity intolerance R/T O2 in blood & tissues Fluid volume excess with CHF
CONT………. Altered nutrition : Less than body requirement R/T excessive energy demands Increased Potential for infection R/TCHF Anxiety related to procedures & hospitalization Developmental delay R/T energy , inadequate nutrition Alterations in parenting
USEFUL HINTS Large male baby with rapid, shallow abdominal breathing: D-TGA Upper body blue, lower body pink; seen in : D-GA+PDA.COA Only cyanotic newborn who has a thrill: Tricuspid atresia. Ejection click is often heard in : Severe PS, HLHS Systolic ejection murmurs in first hours of life: TOF, PS, AS Silent heart characteristic of : D-TGA, Pulmonary atresia. Pulse oximetry& ABG should be obtained from the RIGHT arm. ECG showing LEFT axis deviation: Tricuspid atresia