بسم هللا الرحمن الرحيم. The cardio vascular system By Dr.Rawa Younis Mahmood

Transcription

1 بسم هللا الرحمن الرحيم The cardio vascular system By Dr.Rawa Younis Mahmood

2 Introduction Evaluation of the cardio vascular system depend on history and physical examination by : Asking about cyanosis,blueness during exercise,easy fatigability during feeding,orthopnoea,nocturnal dyspnoea,history of chest pain,palpitation,syncopal attack. 2

3 Physical examination By assessment of growth and development,signs of respiratory distress,to look for oedema presacral or leg oedema,clubbing of fingers,cyanosis if central or peripheral, Vital signs :pulse,blood pressure (cuffs size 3-,5-,7-,12-,18 cm),tempretaure,respiratory rate,heart rate,capillary refill,pulse oxymetry) Jugular venous pulse Systemic examination : The precordium Other systems 3

4 genital heart disease valence :CHD affect 8/1000 live births at th,vsd is the commonest lesion [25-30%] followed rder of decreasing frequency by PDA,TOF,ASD arctation of aorta,tga and endocardial cushion fect. 4

5 Etiology 1.is unknown in most cases 2.genetic factors play some role e.g. VSD. Polygenic inheritance is the commonest type. 3.Environmental factors or adverse maternal conditions and teratogenic effects. CHD.are associated with extra cardiac malformations in[20-45%] of infants and between [5-10%] have known chromosomal abnormalities. 5

6 Classification of CHD CHD.can be divided into two major groups : 1.Acyanotic. 2.Cyanotic. Acyanotic CHD :are divided into 2 groups: 1.Acyanotic CHD with increase volume load as ASD, VSD,AV canal defect and PDA. 2.Acyanotic CHD with increase pressure load as valvular pulmonary stenosis,valvular aortic stenosis and coarctation of aorta. Cyanotic CHD :are divided into two groups: 6

7 Cyanotic CHD: 1.Cyanotic CHD with decrease pulmonary blood flow [RT to LT] shunt as TOF, Tricuspid atresia, single ventricle with pulmonary stenosis.2.cyanotic CHD with increase pulmonary blood flow :here cyanosis caused by either abnormal ventricular or atrial connection or by abnormal total mixing of systemic venous and pulmonary venous blood within the heart as TGA. 7

8 Total mixing lesion include :patients with common atrium or ventricle,total anomalous pulmonary venous return and Truncus arteriosus. 8

9 Acyanotic CHD: ASD The majority of cases are sporadic,however autosomal dominant inheritance occurs as part of HOLT ORAM syndrome. 9

10 Types of ASD 1. Sinus venosus ASD: The defect is located in the upper part of the atrial septum in close relation to the entery of superior vena cava [SVC] and it is similar to ASD secondum in its clinical picture and diagnosis.it can also diagnosed by C-Tscan or MRI of the chest > 10

11 2.Osteium secondum ASD: It is located in the region of fossa ovalis and it is the commonest type of ASD. Pathophysiology of Osteium secondum ASD: Oxygenated blood flows from [LT] to [RT] atrium this blood with that of systemic venous return pass to the [RT] ventricle to be pumped to the lungs. In infants the shunt is minimal so the condition is asymptomatic,but it increases with age to produce the symptoms. 11

12 Clinical picture of ASD secondum: Symptoms: 1.Often asymptomatic,even large ASD rarely produce heart failure. 2.In young children, there may be subtle failure to thrive. 3.In older children there may be variable degrees of exercise intolerance. 12

13 Signs of ASD secondum: 1.[RT] ventricular systolic lift usually palpable at left sternal border. 2.Loud S1,some times pulmonary ejection click with wide and fixed splitting of S2 in all phases of respiration.with systolic ejection murmur at the [LT] upper and middle sternal border. 3.there may be short mid diastolic rumbling murmur at the [LT] lower sternal border due to large volume of blood that flows across the tricuspid valve. 13

14 ASD investigation : 1.CXR:it shoes variable degree of [RT] ventricular and [RT] atrial enlargement, depending on the size of the shunt,the pulmonary artery and vascularity of the lungs are increased. 2.ECG:it may shows [RT] axis deviation &[RT] bundle branch block with [RT] ventricular over load. Echocardiogram :will confirm the diagnosis. 14

15 ASD Complications: 1.Pulmonary hypertension. 2.Atrial dysrrhythemias. 3.Tricuspid or mitral valves insufficiency. 4.Heart failure. 5.Infective endocarditis is extremely rare & antibiotic prophylaxis is not needed. 15

16 ASD Treatment: Is surgical closure when pulmonary to systemic flow ratio=p:s ratio is more than 2:1 it is done between 1-6 years of age. 16

17 ASD Osteium primum defect: The lesion is situated in the lower part of the atrial septum & overlies mitral & tricuspid valves which usually have some structural abnormalities. 17

18 Partial anomalous pulmonary venous return (PAPVR ) One or several pulmonary veins may returns anomalously to the SVC,(RT) atrium or coronary sinus and produce a(lt) to (RT) shunt of oxygenated blood. PAPVR usually involving some or all of the veins from only one lung more often the RT one.when an associated ASD were present it is generally of the sinus venosus type although can be the secondum type. When an ASD detected by echo one must always search 18 for an associated PAPVR.

19 Partial anomalus pulmonary venous return The history,physical signs and ECHO and CXR are indistinguishable from those of secondum ASD. Occasionally an anomalous vein draining into the inferior vena cava is visible on CXR as crescentic shadow of vascular density along the RT border of he cardiac silhoutte (Scimitar syndrome ). in these cases an ASD is not usually present,but pulmonary sequestrations and anomalous arterial supply to that lobe are common findings 19

20 Atrio ventricular septal defect [endo cardial cushion defect] [A-V canal defect] It consist of contagious ASD & VSD with markedly abnormal AV valves,this lesion is common in children with down syndrome. 20

21 Acyanotic congenital heart disease Ventricular septal defect VSD 21

22 VSD VSD account for 25-30% of CHD the majority are of memberanous type. 22

23 23 Anatomy of VSD

24 The pathophysiology of VSD The physical size of the defect is not only the determinant factor of LT to RT shunt but also on the level of pulmonary vascular resistance compared with systemic vascular resistance, after birth PVR may remain higher than normal,thus the size of LT to RT shunt may be limited, as PVR falls in the first few weeks after birth because of the normal involution of the media of small pulmonary arteries &arterioles the size of the shunt increase & the clinical sighns & symptoms appear. 24

25 Pathophysiology of VSD If the LT to RT shunt is large,flow ratio >2.5:1 LT atrial &ventricular overload occur as well as RT ventricle & pulmonary artery hypertension. When the ratio of P:S resistance reach 1:1 the shunt become bidirectional & signs of heart failure abate& the patient become cyanotic [Eisenmenger syndrome]. 25

26 Clinical manifestation of VSD 1.Small VSD: Symptoms: it is usually asymptomatic. Signs : 1.systolic thrill along the lower sternal border. 2.harsh loud or blowing holosystolic (pan) systolic murmur heard best at the LT sternal border. In neonate: short apical systolic murmur. 26

27 Clinical manifestation of large VSD Symptoms : include dyspnoea,feeding difficulties poor growth, profuse sweating, recurrent chest infection & cardiac failure early in infancy. Signs : 1.Prominance of LT precordium. 2.palpable parasternal lift,laterally displaced apex & systolic thrill. 3.Holosystolic murmur less harsh than that of small VSD,there may be mid diastolic murmur. 27

28 Investigation Small VSD 1.CXR:is normal. ECG: is normal. Echocardiography : is difficult to see small VSD unless by color Doppler examination &pulsed Doppler will measure the pressure gradient across the defect. 28

29 Large VSD 1.CXR:cardiomegally,increased pulmonary markings, pulmonary edema &some times pleural effusion. ECG :biventricular hypertrophy,p wave may be notched or peaked. ECHO : will confirm the diagnosis. 29

30 Prognosis of VSD Small VSD:30-50%close spontaneously in the first 2 years& rarely up to 4 years. Large VSD if not closed surgically will progress to congestive heart failure& other complications. 30

31 Treatment of VSD 1.Reassurance of parents. 2.Prophylaxis against SBE in any dental or urinary instrumentation. 3.Treatment of complication as repeated chest infection& heart failure. The real treatment is by surgical closure of the defect. 31