1. VALVULAR HEART DISEASE
SUBJECT: PHYSIOTHERAPY IN
CARDIOPULMONARY CONDITIONS (BPT 402)
SUBMITTED TO: DR. JAMAL MOIZ
SUBMITTED BY: MEHPARA KHAN
BPT 4TH YEAR
JAMIA MILLIA ISLAMIA
Centre for Physiotherapy and Rehabilitation Sciences
1
2. • VHD is groups of critical clinical conditions involve heart valves, leading to
different pattern of dysfunction
• An acquired or congenital disorder of a cardiac valve characterized by stenosis
(obstruction) or regurgitation (backward flow) of blood.
• These conditions 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.
CLASSIFICATION
1. Mitral Stenosis
2.Mitral regurgitation
3. Aortic Stenosis
4.Aortic regurgitation
5.Tricuspid Stenosis
6.Tricuspid regurgitation
7.Pulmonary Stenosis
8.Pulmonary regurgitation
3. THE VALVE OPENING NARROWS:
-The valve leaflets may become fused or thickened that the valve cannot open freely,
obstructs the normal flow.
-The chamber behind the stenotic valve is subject to greater stress, must generate more
pressure to force blood through the narrowed opening
-initially, the heart compensates for the additional workload by gradual hypertrophy and
dilation of the myocardium, finally ending in heart failure
LEAKAGE OR BACKFLOW OF BLOOD RESULTS FROM
INCOMPLETE CLOSURE OF THE VALVE
Due to: scarring and retraction of valve leaflets Or Weakening of
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 dilation and hypertrophy eventually leads to heart failure
5. CLINICAL FEATURES
• Mild or moderate stenosis: usually asymptomatic
• Fatigue & exertional dyspnea
• Chest pain (angina)
• Exertional syncope,
• Weakness, orthopnea, pulmonary edema (severe cases).
• Sudden death
FINDINGS
• harsh, rough, mid-systolic murmur
• Vibration felt over the base of the heart (caused by turbulent blood flow)
• ECG and echocardiogram– LV hypertrophy
• Cardiac catheterization
• 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.
6. MANAGEMENT
• Patients with AS who are asymptomatic should be followed up with serial clinical
examinations, 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 treatment – surgical replacement of aortic valve
• (Ross procedure)
•Balloon valvuloplasty (symptomatic patients who are not surgical candidates)
Balloon valvuloplasty
7.
8. SYMPTOMS
• Acute AR leads to an abrupt onset of symptoms, including dyspnea and chest
pain. Chronic AR, however, is often initially asymptomatic due to the gradual
nature of the resultant LV enlargement.
Signs of LVfailure –
Exertional dyspnea, Fatigue, orthopnea, Chest pain, head ache
Arterial pulsations visible or palpable at the carotid or temporal arteries.
FINDINGS
• High- pitched diastolic murmur at the 2nd/3rd ICS at the left sternal border.
• Diagnosis– confirmedbyECG,echo,andcardiac catheterization
9. 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.
10. 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
PATHOPHYSIOLOGY
11. SYMPTOMS:-
• Breathlessness, cough (pulmonary congestion)
• Chest pain (pulmonary hypertension)
• Hemoptysis (pulmonary congestion or hypertension)
• Fatigue (low cardiac output)
• edema, ascites (right heart failure)
• Palpitation (atrial fibrillation)
SIGNS:-
• Pulse: Weak and irregular due to Atrial fibrillation.
• Mitral facies :(abnormal flushing of the cheeks that occurs from cutaneous vasodilation)
• Auscultation:- Mid-diastolic murmur (apex)
• Crepitation, pulmonary edema, effusions (raised pulmonary capillary pressure)
CLASSIFICATION - NORMAL– 4 to 6cm2
• Mild :- Valve area of 1.6-2.0 cm2
• Moderate :- Valve area of 1-1.5 cm2
• Severe :- Valve area of 1 cm2 orless
12. MANAGEMENT
• Medical management includes:- anticoagulant (To reduce the risk of systemic
embolism) Digoxin, beta blockers, or rate limiting calcium antagonists (To
control ventricular rate in atrial fibrillation) Diuretic (Tocontrol pulmonary
congestion)
• Surgicalmanagementincludes:-Mitral balloon valvuloplasty, Mitral valvotomy,
Valve replacement.
• If the patient is symptomatic or in case of severe MS, surgery is needed.
Valvuloplasty – open/ closed mitral commissurotomy (fused commissures of
the mitral valve are opened)
13. 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 LVinto
LA
Causes:- Tear, shortening or elongation Of Valve leaflets, Chordae tendinae, Annulus,
Papillary muscles.
PATHOPHYSIOLOGY:-
• In acute MR, the LV afterload decreases significantly and the ventricle does
not have adequate time to dilate, resulting in a reduced end diastolic
ventricular volume.
• If the regurgitation persists, 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
output decreases, and the patient clinically decompensates. Severe MR
increases left atrial pressures and pulmonary venous pressures to a lesser
extent than MS.
14. CLINICALFEA
TURES
• Fatigue,W
eakness,Palpitations,Cough,Paroxysmal nocturnaldyspnea,Lowerextremity edema,Syncope,
Atrialfibrillation, v
e
n
t
r
i
c
u
l
a
renlargement,DecreasedB
P
Investigations
ECG: Left atrial enlargement and atrial 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.
MANAGEMENT
• Medical treatment includes Vasodilators (e.g. ACE inhibitors), Diuretics
• If atrial fibrillation presents,
• Anticoagulant
• Digoxin
• Surgical treatment includes:Mitral valve repair OR replacement
15. TRICUSPID STENOSIS
• Isolated tricuspid stenosis (TS) is uncommon. Rheumatic disease is also the most common
cause for TS, which is often accompanied by AS and MS. Other rare causes of TS include
tricuspid atresia, right atrial tumors, and carcinoid syndrome
Symptoms:
• symptoms of right-sided heart failure:- Hepatomegaly, Ascites, Peripheral edema, Neck vein
engorgement
• decrease co – fatigue,hypotension
Signs- Raised JVP, Mid-diastolic murmur (best heard at lower left or right sternal edge).
MANAGEMENT
• Patients with TS are typically 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.
16. Tricuspid regurgitation
• TR often occurs secondary to left-sided valvular disease, which increases right-sided
cardiac volume and pressure.
• The most common cause of TR is dilation of the right ventricle and the tricuspid
annulus, causing poor coaptation of valve leaflets.
C/F
• Hepatic congestion
• Abdominal distention, ascitis
• Generalized edema & weakness
• Low urine out put
• Raised JVP
• Visible veins
• Peripheral edema
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 symptom management.
– Surgical management- Tricuspid valve repair-Annuloplasty
17. 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 a dilated aorta.
• Congenital pulmonic stenosis is managed by balloon dilation.
• Pulmonic regurgitation (PR) is usually caused by dilation of the annulus secondary
to pulmonary hypertension or dilation of the 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.
18. REFERENCES:-
• Mrsic, Z., Hopkins, S. P., Antevil, J. L., & Mullenix, P. S. (2018).
Valvular Heart Disease. Primary Care: Clinics in Office Practice,
45(1), 81–94.
• Valvular Heart Disease: Diagnosis and Management Kameswari
Maganti, MD, Vera H. Rigolin, MD, Maurice Enriquez Sarano, MD,
and Robert O. Bonow, MD
• Valvular Heart Disease: Review and Update BENJAMIN SHIPTON,
D.O., Mercer, Pennsylvania HANEY WAHBA, M.D., Mercy Hospital
of Pittsburgh, Pittsburgh, Pennsylvania
• Valvular Heart Disease: Classic Teaching and Emerging Paradigms D.
Marshall Brinkley, MD, Eli V. Gelfand, MD Beth Israel Deaconess
Medical Center (Cardiovascular Division) and Harvard Medical
School, Boston, Mass.
