VALVULAR HEART DISEASES.pptx gggggghhhhhhhhh

Hematological principles

1. College of Health Sciences Department of Surgery TOPIC: VULVULAR HEART DISEASE PRESENTERS: DR. OGWANG OSCAR TUTOR: DR PHIONA BUKIRWA

2. CONTENTS INTRODUCTION STENOSIS REGURGITATION AOTIC STENOSIS AORTIC INSURFICIENCY MITRAL STENOSIS MITRAL INSUFFICIENCY TRICUSPID STENOSIS TRICUSPID INSURFICENCY PULMONARY VALVE DISEASE

3. VALVULAR HEART DISEASE VHD is groups of critical conditions involve heart valves, leading to different pattern of dysfunction. An acquired or congenital disorder of a cardiac valve characterise by stenosis(obstruction) or regurgitation(backward flow) of blood. These condition occur largely as a consequence of aging, but may also be the result of congenital(inborn) abnormalities or specific disease or physiologic processes including rheumatic heart disease and pregnancy.

4. CLASSIFICATION Mitral Stenosis. Mitral Regurgitation. Aortic Stenosis. Aortic Regurgitation Tricuspid Stenosis Tricuspid Regurgitation Pulmonary Stenosis. Pulmonary Regurgitation

5. THE VALVULAR OPENING NARROWS The valve leaflets may become fused or thickened that the valve cannot open freely obstructing the normal flow. The chamber behind the stenotic valve is subjected to greater stress, must generate more pressure to force blood through the narrow opening. Initially, the heart compensates for the additional workload by gradual hypertrophy and dilation of the myocardium, finally ending in heart failure.

6. LEAKAGE OR BACKFLOW OF BLOOD RESULTS FROM INCOMPLETE CLOSURE OF THE VALVE Due to: scaring and restriction of the valve leaflets or weakening of the supporting structures. Causes the heart to pump the same blood twice(as the blood comes back into the chamber) The heart dilates to accommodate more blood. Ventricular dilatation and hypertrophy eventually leads to heart failure.

7. AORTIC STENOSIS Etiologic Factor. Congenital malformation of the valve. Calcification of normal trileaflet valve and Rheumatic heart disease.

8. CLINICAL FEATURES Mild or moderate stenosis: usually asymptomatic. Fatigue and exertional dyspnea Chest pain(angina) Exertional syncope, Weakness, orthopmea , pulmonary edema (severe cases) Sudden death.

9. FINDINGS Harsh, rough, mid-systolic murmur. Vibration felt over the base of the heart(caused by turbulent blood flow) ECG and echocardiogram-LV hypertrophy. Doppler echocardiography is an excellent tool for both evaluating the severity of As by measuring jet velocity and gradients and calculating the aortic valve area.

10. MANAGEMENT Patients with AS who are asymptomatic should be followed up with serial clinical examination and careful attention should be paid to any change in symptoms. Moderate/severe stenosis evaluated every 1-2 years with doppler echocardiography( to detect progression in severity) Definitive management- surgical replacement of the aortic valve(Ross procedure) Balloon valvuloplasty(symptomatic patients who are not surgical candidates)

11. AORTIC REGURGITATION Etiology Aortic regurgitation results from abnormalities of the aortic leaflets, their supporting structures in the aortic root and annulus, or both, rheumatic heart disease remains the most common cause of severe AR worldwide.

12. SYMPTOMS Acute AR leads to an abrupt onset of symptoms, including dyspnea and chest pain, Chronic AR, however, is often initially asymptomatic due to gradual nature of the resultant LV enlargement SIGNS OF LV FAILURE . Exertional dyspnoea, fatigue, orthopnoea, chest pain, headache. Arterial pulsations visible or palpable at the carotid or temporal arteries. FINDINGS High-pitched diastolic murmur at the 2 nd /3 rd ICS at the left sternal border. Diagnosis-confirmed by ECG, Echo and cardiac catherization

13. MANAGEMENT Asymptomatic patients with severe AR and normal LV size and function should undergo clinical examination and echocardiography yearly unless symptoms arise beforehand. In patients with chronic aortic regurgitation, surgery should be performed before the ejection fraction falls below 55 percent or the end systolic dimension exceeds 55 mm. Systolic BP should be controlled with vasodilating drugs, such as nifedipine or ACE inhibitors.

14. MITRAL STENOSIS Most common valvular disorder in Rheumatic endocarditis. May also be caused by bacterial infection, thrombus formation, calcification. Obstruct blood flow from left atrium to the left ventricle.

15. SYMPTOMS Breathlessness cough (pulmonary congestion) Chest pain (pulmonary hypertension) Haemoptysis (pulmonary congestion or hypertension). Fatigue low cardiac output) Edema , ascites(right heart failure) Palpitation(atrial fibrillation)

16. SIGNS Pulse: Weak and irregular due to Atrial fibrillation Mitral facies : abnormal flushing of the cheeks that occur from cutaneous vasodilation) Ausculatation :-Mid-diastolic murmur(Apex) Crepitation, pulmonary edema , effusions(raised pulmonary capillary pressure)

17. MANAGEMENT Medical management includes:-anticoagulant, Digoxin,beta blockers or rate limiting calcium antagonist(to control ventricular rate in artrial fibrillation) Diuretic(to control pulmonary congestion) Surgical Management includes:- Mitral balloon valvuloplasty, mitral valvotomy, valve replacement. If the patient is symptomatic or in case of severe MS, Surgery is needed.

18. MITRAL REGURGITATION Incomplete closure of mitral valve, the margins of the valves are unable to close completely during ventricular systole leading to back flow of blood from LV to LA Causes:-Tear, shortening or elongation of valve leaflets, chordae tendinae , Annulus, papillary muscles. PARTHOPHYSIOLOGY:- In acute MR, the LV afterload decreases significantly and the venticles does not have adequate time to dilate, resulting in a reduced end diastolic ventricular volume.

19. Cont If the regurgitation persist, the left ventricle dilates through the process of eccentric hypertrophy, allowing the end diastolic volume to increase. As the dilation becomes too great, the ejection fraction decreases, cardiac ouput decreases, and the patient clinically decompensates, severe MR increases left atrial pressures and pulmonary venous pressure to a lesser extend than MS.

20. Clinical features Fatique , weakness, palpitation,cough , paroxysmal nocturnal dysnea , lower extremity edema , sycope , Atrial fibrillation, ventricular enlargement, Decrease BP, INVESTIGATION ECG: left atrial enlargement and atril fibrillation are the most common ECG findings in patients with MR. Left ventricular enlargement is noted in approximately one third of patients. ECHO:-dilated LA,LV.

21. MANAGEMENT Medical treatment includes vasodilators( e.g ACE inhibitors) Diuretics, If atrial fibrillation presents, Anticoagulant Digoxin Surgical treatment includes: mitral valve repair or replacement

22. TRICUSPID STENOSIS Isolated tricuspid stenosis is uncommon, Rheumatic heart disease is the most common cause of TS, which is often accompanied by AS and MS, other rare causes of TS includes tricuspid atresia, right atrial tumors and carcinoid sundrome . SYMPTOMS Symptom of right sided heart failure: Hepatomegaly,ascites , peripheral edema , neck vein enlargement. Decrease CO-fatigue, hypotension SIGNS:-Raised JVP, Mid-diastolic murmur(best heard at lower left or right sternal adge )

23. MANAGEMENT Patients with TS are typicaly managed with salt restriction and diuresis. In the absence of TR, patients with severe symptomatic TS can undergo percutaneous balloon commissurotomy. Because most patients have concomitant valvular regurgitation, tricuspid valve surgery is more commonly pursued for that indication.

24. TRICUSPID REGURGITATION TR often occurs secondary to left-sided valvular disease which increases right sideded cardiac volume and pressure. The most common cause of TR is dilatation of the right ventricles and tricuspid annulus, causing poor coaptation of valve leaflets. C/F Hepatic congestion Abdominal distension, ascites Generalised edema and weakness Low urine output Raised JVP Visible veins Peripheral edema .

25. MANAGEMENT Patients without coexisting pulmonary hypertension usually tolerate regurgitation through the tricuspid valve reasonably well. When signs or symptoms of right sided heart failure develop, diuretics are first line agents for symptoms management. Surgical management-Tricuspid valve repair-Annuloplasty.

26. PULMONIC VALVE DISEASE Most cases of pulmonic stenosis are congenital in Origin Other causes include rheumatic, carcinoid and cardiac tumor obstruction and external compression by dilated aorta. Congenital pulmonic stenosis is managed by balloon dilatation Pulmonic regurgitation is usually caused by dilation of the annulus secondary to pulmonary hypertension or dilation of pulmonary artery Infective endocarditis can also cause PR. An increasingly common cause of PR occurs in adults with congenital disease, such as tetralogy of fallot , that was previously surgically corrected. Treatment of PR is Usually aimed at treating the cause of the pulmonary hypertension, right heart failure or Volume overload. Surgery or percutaneous approaches are used for patients with previously corrected congenital disease.