Download Free Medical Approach to Cyanotic Congenital Hear Disease PowerPoint Presentation

Approach to Cyanotic Congenital Hear Disease PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "APPROACH TO CYANOTIC CONGENITAL HEART DISEASE" by Punit Goel, MD.

This medical PowerPoint presentation talks about Cyanotic congenital heart disease (CCHD).

Cyanotic congenital heart disease (CCHD) is a group of heart defects that result in decreased oxygenation of the blood and can cause cyanosis, a bluish discoloration of the skin, lips, and nails.

The approach to CCHD typically involves a thorough evaluation of the patients medical history, physical examination, and diagnostic testing, such as echocardiography, electrocardiogram, and cardiac catheterization.

Treatment options for CCHD depend on the specific type and severity of the heart defect. In some cases, surgery may be necessary to repair or correct the defect. In other cases, medications may be used to alleviate symptoms and improve heart function.

It is essential to monitor and manage the patients oxygen levels, as well as any related medical conditions, such as anemia, that may exacerbate the symptoms of CCHD.

Lifelong follow-up with a healthcare professional who specializes in congenital heart disease is typically recommended to manage symptoms and monitor for potential complications. Newer therapeutic options like genetic therapy and stem cell therapy are under development and hold promise for future improvement in the management of CCHD.

Tags : Cyanotic congenital heart disease, CCHD, cyanosis, cardiology, cardiology PowerPoint presentation

Published on : Mar 17, 2023 | Views : 1792 | Downloads : 6

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

APPROACH TO CYANOTIC CONGENITAL HEART DISEASE Dr. R. Suresh Kumar Head, Department of Pediatric Cardiology
Slide 2-

Cyanosis Bluish discolouration of skin & mucous membranes due to increased concentration of reduced Hb >3g% ABG; >5g%CBG Causes— CNS, Musculoskeletal system, Airways, Alveolar-capillary membrane, Hb AND CVS. Central vs peripheral. Cardiac vs Respiratory. Peaceful cyanosis is cardiac
Slide 3-

Evaluation of the cyanotic baby Is the baby cyanosed? SpO2 will confirm. Is the cyanosis central/peripheral? Keep the baby warm. Is cyanosis cardiac? 1)Respiratory distress 2)Response to oxygen ABG - low pH, low pO2, Low pCo2 CxR-heart size & configuration, vascularity ECG Axis RV/LV dominance
Slide 4-

Cyanotic CHD-classification Reduced Pulmonary blood flow Tetralogy of Fallot/pulmonary atresia TOF-like physiology (complex congenital heart disease, large VSD PS/PA) Critical PS/ pul.atresia intact IVS Ebstein’s anomaly Low pAO2, oligaemic lungs, neonates respond to PGE1.
Slide 5-

Classification - Cyanotic CHD, Increased PBF Transposition of Great Arteries Total Anomalous Pulmonary Venous connection Single Ventricle Truncus Arteriosus DORV
Slide 6-

Clinical findings CCHD with decreased pulmonary blood flow Quiet precordium Single S2 Murmurs Ejection systolic murmur at the base No murmur Continuous murmur of PDA / collaterals ECG – RAD, RVH LV dominance in tricuspid atresia LAD in tricuspid atresia, AVCD with PS, Single ventricle with PS
Slide 7-

Clinical findings - 2 CCHD with increased pulmonary blood flow Mild cyanosis Active precordium Epigastric pulsations Congestive heart failure Single S2 (except in TAPVC) TGA Profound cyanosis Single S2 No murmur Normal / mildly increased lung vascularity on CXR
Slide 8-

Tetralogy of Fallot/P.Atresia Large VSD/ RVOT obstruction/atresia Cyanosis depends on degree of Obstruction, PDA/collaterals Neonates may need PGE1 to maintain saturation – needs urgent BT shunt. Progressive cyanosis/spells Total correction-around 1 yr.
Slide 9-

ppt slide no 9 content not found
Slide 10-

ppt slide no 10 content not found
Slide 11-

Cyanotic Spells Rapid decrease in systemic oxygen saturation with hyperventilation  Convulsions, coma, death. Age : 6mon – 6 yrs. Cyanosis on crying is not a spell. Crying/exercise may trigger spells. Drop in SVR/ Inf.spasm  R to L shunt  acidosis  hyperventilation :vicious cycle
Slide 12-

ppt slide no 12 content not found
Slide 13-

Cyanotic Spell- Treatment Knee chest position , Oxygen Morphine 0.1 mg/kg iv (sedation,resp dep.);Soda bicarb iv 1-2 ml/kg Increase SVR : Propranolol 0.1 mg/kg iv; Methoxamine 0.1 mg/kg iv; Phenylephrine 1-5mic.g/kg /min iv infusion. Ventilation. Paralyse Emergency surgery Propranolol for prophylaxis
Slide 14-

ppt slide no 14 content not found
Slide 15-

Complex CHD,TOF-like physiology DORV PS/PA Presents like TOF. Needs neonatal BT shunt, if ductus-dependent. Total correction around 1 year, may need a homograft. Single Ventricle PS/PA. Presents like TOF. But 2-ventricle Repair not possible.Neonatal BT shunt, if needed. SVC to RPA anastomosis (Bidirectional Glenn) at 3-6months. IVC to PA connection (Lateral tunnel or Extra cardiac Fontan) at 2-5 yrs.
Slide 16-

ppt slide no 16 content not found
Slide 17-

Tricuspid Atresia Pulmonary blood flow depends on ASD, VSD, Pulmonary stenosis. May be increased / decreased / balanced. Cyanosis or heart failure predominant presentation accordingly. LV dominance and left axis in ECG helpful. Management in Fontan track.Neonatal BT shunt (for severe cyanosis) or PA banding (for heart failure) may be needed.
Slide 18-

ppt slide no 18 content not found
Slide 19-

ppt slide no 19 content not found
Slide 20-

ppt slide no 20 content not found
Slide 21-

Critical PS PAIVS Cyanosis on day 1. Pulmonary circulation ductus dependent. RV normal or in a range of hypoplasia. If RV is adequate,catheter or surgical pulmonary valvotomy is the treatment. If RV is small, BT shunt. May need both. Further management may be - Glenn + Pulm. Valvotomy (1½ ventricle) or staged Fontan, when 2-ventricle repair not possible. Myocardial sinusoids / RV dependent coronary circulation - adverse prognosis.
Slide 22-

ppt slide no 22 content not found
Slide 23-

ppt slide no 23 content not found
Slide 24-

Ebstein’s anomaly Inferior displacement of septal and inferior tricuspid leaflets. Thin RV. May have PS. Neonatal cyanosis may be severe. High PVRTR  R to L atrial shunt. Usually transient. Course:May be asymptomatic. Cyanosis, Rt heart failure and SVT may be problems. Surgery for severe cyanosis/heart failure.
Slide 25-

Ebstein’s anomaly History of SVT Generally good effort tolerance Cardiomegaly Multiple heart sounds (split S1, split S2, S3, S4) Scratchy systolic murmur at LLSB Cardiomegaly with huge RA on CxR. ECG-abnormal axis, RAE, polyphasic QRS. May have WPW syndrome
Slide 26-

ppt slide no 26 content not found
Slide 27-

ppt slide no 27 content not found
Slide 28-

Cyanotic CHD, increased PBF. Transposition of GA Commonest cyanotic CHD on day 1. Aorta from RV, PA from LV. Presentation depends on Intact IVS, VSD, PS. TGA intact IVS. Cyanosis on Day1. No murmur. CxR- egg on side heart,normal vascularity. Untreated 90% die in first month, if no ASD. Management : PGE1 till Balloon Atrial Septostomy. Arterial Switch Operation in first month. Good long-term result.
Slide 29-

ppt slide no 29 content not found
Slide 30-

ppt slide no 30 content not found
Slide 31-

ppt slide no 31 content not found
Slide 32-

TGA with VSD No PS: Cyanosis minimal. CHF in a few weeks. Needs Arterial Switch operation in 3 months. Rapid progression of PVD, if untreated. TGA/VSD/PS: Cyanosis depends on degree of PS. BT shunt if cyanosis is severe. Rastelli operation at 3-5 yrs.
Slide 33-

TAPVC All 4 pulm veins join a common chamber which eventually reaches RA. Supracardiac- common chamber drains to innominate vein or to SVC. Cardiac- drains to coronary sinus or RA Infracardiac (Infradiaphragmatic). Descending vertical vein  portal vein  ductus venosus  IVC. Obstructed.
Slide 34-

ppt slide no 34 content not found
Slide 35-

TAPVC-2 Obstructed venous return: Presents with pulmonary oedema. Infradiaphragmatic on Day1, supracardiac in a fewdays. Emergency surgery life saving. Normal life span. Unobstructed: Cardiac, some supracardiac. Slow onset of CHF, minimal cyanosis. Clinical features of ASD Figure of 8 cardiac silhouette on CxR. Good surgical results.
Slide 36-

ppt slide no 36 content not found
Slide 37-

ppt slide no 37 content not found
Slide 38-

Persistent Truncus Arteriosus A single arterial trunk leaves the heart above a VSD. PA arises with a common trunk or as separate branches. CHF in a few weeks of life, mild cyanosis. Bounding pulses,systolic click and murmur. EDM, if truncal valve is incompetent. CxR - CE, High origin of PA branches,increased vascularity. Surgical Repair in first month preferred.
Slide 39-

ppt slide no 39 content not found
Slide 40-

Cyanotic CHD in older children and adults Tetralogy of Fallot Commonest CCHD with reduced pulmonary blood flow surviving into adulthood Exertional dyspnoea and squatting Varying degrees of cyanosis Eisenmenger syndrome History of recurrent respiratory infections in early childhood Good effort tolerance till late in the nature history Mild cyanosis Findings of severe pulmonary artery hypertension
Slide 41-

Eisenmenger VSD Presents in second decade Single S2 Normal heart size on CXR Dilated central pulmonary arteries with peripheral pruning
Slide 42-

Eisenmenger PDA Presents in second or third decade Differential cyanosis and clubbing Normally split S2 with loud P2 Normal heart size on CXR Dilated central pulmonary arteries with peripheral pruning
Slide 43-

Eisenmenger ASD Presents in fourth or fifth decade Cardiomegaly Widely split S2 Atrial fibrillation
Slide 44-

Thank You