Congenital heart disease,anesthetic management

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Congenital heart disease,anesthetic management

  1. 1. CONGENITAL HEART DISEASE AND ANESTHETIC MANAGEMENT By Dr.A.Sattar Dept;of Anesthesia,SIUT Karachi
  2. 2. Congenital anomalies of heart and Cardiovascular System – <ul><li>Incidence – 1% (10 per 1000 live births). </li></ul><ul><li>30% of the total incidence of all congenital diseases. </li></ul><ul><li>More than 100 different CHD recognized. </li></ul><ul><li>90% CHD can be placed in 9 Categories. </li></ul><ul><li>Remaining 10% are more unusual and complex congenital heart lesions. </li></ul>
  3. 3. COMMON CONGENITAL HEART DISEASES - <ul><li>Disease Incidence </li></ul><ul><li>ACYANOTIC DEFFECTS - </li></ul><ul><li>Ventricular Septal Defect (VSD) - 30% </li></ul><ul><li>Atrial Septal Defect (ASD) - 10% </li></ul><ul><li>Patent Ductus Arteriosus (PDA) 10% </li></ul><ul><li>Pulmonary Stenosis - 10% </li></ul><ul><li>Aortic Stenosis - 7% </li></ul><ul><li>Coartation of the aorta - 5% </li></ul><ul><li>Atrioventricular Septal Defect - 3% </li></ul><ul><li>CYANOTIC DEFECTS – </li></ul><ul><li>Tetralogy of Fallot - 10% </li></ul><ul><li>Transposition of the great vessels - 5% </li></ul>
  4. 4. ACYANOTIC CONGENITAL HEART DISEASE. <ul><li>Characterized by a left to right intracardiac shunt. </li></ul><ul><li>Ultimate result of this shunt,regardless of its location is: </li></ul><ul><li>increased pulmonary blood flow </li></ul><ul><li>pulmonary hypertension </li></ul><ul><li>right ventricular hypertrophy </li></ul><ul><li>and eventually CCF </li></ul>
  5. 5. ACYANOTIC CONGENITAL HEART DISEASE RESULTING IN A LEFT- TO- RIGHT INTRACARDIAC SHUNT. <ul><li>Secundum Atrial Septal Defect (ASD). </li></ul><ul><li>Primum Atrial Septal Defect (ASD) (Endocardial cushion Defect). </li></ul><ul><li>Ventricular Septal Defect (VSD). </li></ul><ul><li>Aorticopulmonary fenestration. </li></ul>
  6. 6. ATRIAL SEPTAL DEFECT (ASD) <ul><li>1/3 of CHD detected in adults. </li></ul><ul><li>More in females. </li></ul><ul><li>Anatomically an ASD may be devided in: </li></ul><ul><li>Ostium secondum </li></ul><ul><li>most common type </li></ul><ul><li>located in the region of fossa ovalis,in the middle of interatrial septum. </li></ul><ul><li>Ostium primum </li></ul><ul><li>less common </li></ul><ul><li>endocardial cushion defect </li></ul><ul><li>large opening,located in the lower interatrial septum. </li></ul><ul><li>Sinus Venosus </li></ul><ul><li>located at upper interatrial septum. </li></ul>
  7. 7. ATRIAL SEPTAL DEFECT (ASD)
  8. 8. ATRIAL SEPTAL DEFECT (ASD) <ul><li>Physiologic consequences of ASD are the same regardless of anatomic location. </li></ul><ul><li>The shunting of blood from one atrium to the other occurs. </li></ul><ul><li>The direction and magnitude of the shunt are determined by the size of the defect and the relative comlpliance of ventricles. </li></ul><ul><li>A small 0.5cm defect is associated with a small shunt and no haemodynamic problem. </li></ul><ul><li>A 2cm defect result in shunting of blood from left to right and increased pulmonary blood flow. </li></ul>
  9. 9. ATRIAL SEPTAL DEFECT (ASD) <ul><li>SIGNS AND SYMPTOMS </li></ul><ul><li>Initially no symptoms,no physical finding. </li></ul><ul><li>May remain undetected for years. </li></ul><ul><li>Small ASD with ratio of pulmonary to systemic flow of less than 1.5,no closure of ASD required. </li></ul><ul><li>Large ASD,ratio more than 1.5,causes dyspnoea on exertion,supraventricular arrythmias,RHF,paradoxical embolism and recurrent pulmonary infections. </li></ul><ul><li>A systolic ejection murmur is present in 2 nd left intercostal space . </li></ul><ul><li>ECG shows RAD,incomplete RBBB,AF,and SVT in adults. </li></ul><ul><li>CXR shows prominent pulmonary arteries. </li></ul><ul><li>Echocardiography with Doppler color flow is useful for detecting the location of ASD`s. </li></ul>
  10. 10. ATRIAL SEPTAL DEFECT (ASD) <ul><li>ANESTHETIC MANAGEMENT </li></ul><ul><li>In the absence of CCF,no significant alteration in intravenous or volatile anesthetic response. </li></ul><ul><li>Avoid increase in SVR because it will increased magnitude of shunt. </li></ul><ul><li>Decrease in SVR due to volatile anesthetics will decrease magnitude of shunt. </li></ul><ul><li>IPPV will increase PVR that will also decrease the shunt. </li></ul><ul><li>Avoid air entrance in circulation. </li></ul><ul><li>Give prophylactic antibiotics against infective endocarditis if valvular abnormality is present. </li></ul><ul><li>Transient SVT and AV conduction defect may occur in early post operative period after surgical repair of ASD. </li></ul>
  11. 11. VENTRICULAR SEPTAL DEFECT (VSD) <ul><li>The most common CHD in infants and children. </li></ul><ul><li>Large number of VSDs close spontaneously before 2 years of age. </li></ul><ul><li>Anatomically can be divided into: </li></ul><ul><li>Membranous VSD – 70% </li></ul><ul><li>Muscular VSD – 20% </li></ul><ul><li>Others – 10%. </li></ul>
  12. 12. VENTRICULAR SEPTAL DEFECT (VSD)
  13. 13. VENTRICULAR SEPTAL DEFECT (VSD) <ul><li>SIGNS AND SYMPTOMS </li></ul><ul><li>Physiologic significance of VSD depends on size of the defect and the relative resistance in the pulmonary and systemic circulations. </li></ul><ul><li>Small VSD – minimal functional disturbance. </li></ul><ul><li>Large VSD – ventricular pressures equalize and magnitude of flow depends on SVR and PVR. </li></ul><ul><li>Systolic murmur is heard at left lower sternal border. </li></ul><ul><li>ECG shows RAD,RVH and LVH. </li></ul><ul><li>CXR – initially normal. </li></ul><ul><li>Echocardiography and Angiography are diagnostic. </li></ul>
  14. 14. VENTRICULAR SEPTAL DEFECT (VSD) <ul><li>ANESTHETIC MANAGEMENT </li></ul><ul><li>Antibiotic prophylaxis against infective endocarditis. </li></ul><ul><li>Acute and persistent increase in SVR or decrease in PVR are undesirable as these will increase magnitude of shunt. </li></ul><ul><li>The pharmacokinetics of inhaled and injected drugs are not significantly altered by VSD. </li></ul><ul><li>High inspired concentration of volatile anesthetics may cause cardiac depression. </li></ul>
  15. 15. PATENT DUCTUS ARTERIOSUS (PDA) <ul><li>This is present when the ductus arteriosus fails to close spontaneously shortly after birth. </li></ul><ul><li>Ductus arteriosus connects descending Aorta to left pulmonary artery,it closes 24 – 48 hours after birth but in preterms frequently fail to close. </li></ul><ul><li>The result is a left-to-right shunt and increase pulmonary blood flow. </li></ul>
  16. 16. PATENT DUCTUS ARTERIOSUS (PDA)
  17. 17. PATENT DUCTUS ARTERIOSUS (PDA) <ul><li>SIGNS AND SYMPTOMS </li></ul><ul><li>Most patients are asymptomatic. </li></ul><ul><li>Only have modest left-to-right shunt. </li></ul><ul><li>It left-to-right shunt is large it may cause LVH,pulmonary hypertension and RVH. </li></ul><ul><li>If surgical closure is not done most patients remain asymptomatic until adolescence but may develop pulmonary hypertension and CCF. </li></ul><ul><li>In severe pulmonary hypertension surgical and percutaneous closure is contraindicated. </li></ul><ul><li>Often detected during routine physical examination with continuous systolic and diastolic murmur. </li></ul><ul><li>ECG and CXR show LVH. </li></ul><ul><li>Echocardiography with doppler studies confirms the dignosis. </li></ul>
  18. 18. PATENT DUCTUS ARTERIOSUS (PDA) <ul><li>TREATMENT </li></ul><ul><li>Surgical ligation is associated with low mortality and usually CPB is not required. </li></ul><ul><li>In some cases medical closure of PDA with inhibition of prostaglandin synthesis with cox – 1 or cox – 2 appears to be effective as alternative to surgery. </li></ul>
  19. 19. PATENT DUCTUS ARTERIOSUS (PDA) <ul><li>ANESTHETIC MANAGEMENT </li></ul><ul><li>Antibiotic prophylaxis against infective endocarditis. </li></ul><ul><li>Anticipate blood loss. </li></ul><ul><li>Anesthesia with volatile anesthetic and IPPV is useful. </li></ul><ul><li>Artrial BP monitoring is helpful. </li></ul><ul><li>Ligation of PDA is often associated with hypertension in post operative period. </li></ul>
  20. 20. CYANOTIC CONGENITAL HEART DISEASES <ul><li>Characterized by a right-to-left intracardiac shunt with associated decrease in pulmonary blood flow and the development of arterial hypoxemia. </li></ul><ul><li>Chronic hypoxemia results in erythrocytosis and thromboembolism. </li></ul><ul><li>Secondary erythrocytosis may cause coagulation defect. </li></ul><ul><li>Risk of CVA and brain abscess. </li></ul><ul><li>Without surgical treatment patient can not survive to adulthood. </li></ul>
  21. 21. CYANOTIC CONGENITAL HEART DISEASES RESULTING IN RIGHT-TO-LEFT INTRACARDIAC SHUNT <ul><li>Tetralogy of fallot. </li></ul><ul><li>Eisenmenger syndrome. </li></ul><ul><li>Ebtein`s anomally (Tricuspid malformation). </li></ul><ul><li>Tricuspid atresia. </li></ul><ul><li>Foramen ovale. </li></ul>
  22. 22. TETRALOGY OF FALLOT <ul><li>Most common cyanotic CHD. </li></ul><ul><li>Characterized by a large single VSD,an aorta that overrides the right and left ventricles,obstruction to right ventricle out flow and right ventricular hypertrophy. </li></ul><ul><li>TOF with ASD or other anomalies may occur (Pentalogy of fallot). </li></ul><ul><li>Right-to-left entracardiac shunting occurs because of increased resistance to flow in the right ventricular out flow tract. </li></ul><ul><li>Because resistance to flow across the right ventricular out flow tract is relatively fixed,changes in SVR (drug induced) may affect the magnitude of the shunt. </li></ul><ul><li>Decrease in SVR,increase right-to-left intracardiac shunting and increase arterial hypoxemia. </li></ul><ul><li>Increase in SVR decrease right-to-left intracardiac shunting with resultant increase in pulmonary blood flow. </li></ul>
  23. 23. TETRALOGY OF FALLOT
  24. 24. TETRALOGY OF FALLOT <ul><li>DIAGNOSIS </li></ul><ul><li>Echocardiography with color Doppler imaging and spectral Doppler measurement. </li></ul><ul><li>Cardiac catheterization confirms diagnosis,anatomic and hemodynamic data. </li></ul><ul><li>MRI. </li></ul>
  25. 25. TETRALOGY OF FALLOT <ul><li>SIGNS AND SYMPTOMS </li></ul><ul><li>Cyanosis : from birth or start in first year of life. </li></ul><ul><li>CCF : rare because large VSD permits equalibration of intraventricular pressures and cardiac work load. </li></ul><ul><li>Low oxygen saturation : even at 100% oxygen. </li></ul><ul><li>Compensatory erythropoises . </li></ul><ul><li>Squating is common. </li></ul>
  26. 26. TETRALOGY OF FALLOT <ul><li>SIGNS AND SYMPTOMS </li></ul><ul><li>Hypercyanotic attacks </li></ul><ul><li>These are characterized by sudden spells of arterial hypoxemia associated with worsening cyanosis,tachypnoea,loss of consceousness,seizures,CVA and even death. </li></ul><ul><li>This is associated with crying and exercise due to sudden decrease in pulmonary blood flow due to spasm of infundibular cardiac muscle or decrease in SVR. </li></ul><ul><li>Treatment is release of spasm by beta blockers like esmolol or proponolol but if the cause is decrease in SVR then give fluids and phenylephrine. </li></ul><ul><li>Sympathomimetics with beta agonist activity should be avoided because they may cause spasm of infundibular cardiac muscle. </li></ul><ul><li>Recurrent hypercyanotic attacks indicate need for surgical correction of TOF. </li></ul>
  27. 27. TETRALOGY OF FALLOT <ul><li>SIGNS AND SYMPTOMS </li></ul><ul><li>CVA </li></ul><ul><li>Cause is cerebrovascular thrombosis or severe hypoxemia. </li></ul><ul><li>Thrombosis </li></ul><ul><li>Cause is polycythemia and dehydration. </li></ul><ul><li>Cerebral abscess </li></ul><ul><li>Cause is arterial seeding into areas of prior cerebral infarction. </li></ul><ul><li>Infective endocarditis </li></ul><ul><li>associated with high mortality. </li></ul>
  28. 28. TETRALOGY OF FALLOT <ul><li>ANESTHETIC MANAGEMENT </li></ul><ul><li>Avoid increases in PVR or decrease in SVR because these will increase shunt magnitude that will decrease pulmonary blood flow and oxygen saturation. </li></ul><ul><li>SVR is decreased by Volatile anesthetics,Histamine realese,Ganglionic blockade and Alfa adrenergic blockade. </li></ul><ul><li>PVR is increase by High inflation pressures,Peep and acidosis. </li></ul>
  29. 29. TETRALOGY OF FALLOT <ul><li>ANESTHETIC MANAGEMENT </li></ul><ul><li>Preoperative Preparation </li></ul><ul><li>Avoid dehydration,give i/v fluids. </li></ul><ul><li>Avoid crying of patient,don’t give i/m injections. </li></ul><ul><li>Continue beta blockers. </li></ul>
  30. 30. TETRALOGY OF FALLOT <ul><li>ANESTHETIC MANAGEMENT </li></ul><ul><li>Induction of Anesthesia </li></ul><ul><li>Induce with Ketamine 1-2 mg/kg i/v. </li></ul><ul><li>Decrease rate of muscle rexalant dose. </li></ul><ul><li>Induction with volatile anesthetics is slow. </li></ul><ul><li>Sevoflurane and Halothane can be used but with caution and careful monitoring of oxygenation. </li></ul><ul><li>Hypercyanotic attacks may occur. </li></ul>
  31. 31. TETRALOGY OF FALLOT <ul><li>ANESTHETIC MANAGEMENT </li></ul><ul><li>Maintenance of anesthesia </li></ul><ul><li>Can be achieved by Ketamine. </li></ul><ul><li>Nitrous oxide but not more than 50% can be used but disadvantage is mild increase in PVR and decrease in FIO 2. </li></ul><ul><li>Opiods and benzodiazepine can be used in low dose to avoid SVR and BP. </li></ul><ul><li>Muscle relaxation by pancuronium to maintain SVR and BP. </li></ul><ul><li>IPPV – avoid airway pressure and peep. </li></ul><ul><li>Maintain intravascular volume. </li></ul><ul><li>Avoid infusion of air. </li></ul><ul><li>Phenylephrine must be available to treat decrease in BP due to decrease in SVR. </li></ul>
  32. 32. SUMMARY <ul><li>Due to improvement in medical management the more number of CHD patients are encountered in anesthesia for non cardiac surgery. </li></ul><ul><li>These CHD patients may be considered UNREPAIRED,CURED,CORRECTED or PALLIATED. </li></ul><ul><li>Preoperative assessment include good history,physical examination,routine investigations,doppler echocardiography,review of old records,information from primary surgeon/physician and important post operative findings like arrhythmias,hypoxemia,pulmonary hypertension,existing shunts,paradoxical embolism and bacterial endocraditis. </li></ul>
  33. 33. SUMMARY <ul><li>Understand pathophysiology of defects. </li></ul><ul><li>In left-to-right shunts avoid in SVR,infact decrease in SVR and increase in PVR are desireable. </li></ul><ul><li>BUT </li></ul><ul><li>These are fatal in right-to-left shunts. </li></ul><ul><li>So in right-to-left shunts avoid decrease in SVR and increase in PVR. </li></ul>
  34. 34. THANK YOU

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