VALVULAR

HEART DISEASE

JENNY VARGHESE
1ST YEAR MSC NURSING
 OBJECTIVES

At the end of the seminar students will be able to

▪ Define valvular hear disease
▪ Classify valvular hear disease
▪ Enlist causes of valvular hear disease
▪ Enlist clinical manifestations of valvular hear disease
▪ Describe medical and surgical management of valvular hear disease
▪ Explain nursing management valvular hear disease
 Definition
▪ Valvular heart disease is when any valve in the heart has damage or is diseased.
▪ The normal heart has four chambers (right and left atria, and right and left ventricles)
and four valves.
▪ The mitral valve, also called the bicuspid valve, allows blood to flow from the left
atrium to the left ventricle.
▪ The tricuspid valve allows blood to flow from the right atrium to the right ventricle.
▪ The aortic valve allows blood to flow from the left ventricle to the aorta.
▪ The pulmonary valve allows blood to flow from the right ventricle to the pulmonary
artery.
Classification of valvular heart disease

VHD

STENOSIS REGURGITATION
CLASSIFICATION OF VHD

STENOSIS REGURGITATION

▪ MITRAL STENOSIS ▪ MITRAL REGURGITATION

▪ AORTIC STENOSIS ▪ AORTIC REGURGITATION
▪ PULMONARY STENOSIS ▪ PULMONARY
REGURGITATION
▪ TRICUSPID STENOSIS
▪ TRICUSPID REGURGITATION
STENOSIS
THE VALVE LEAFLETS MAY BECOME FUSED OR
THICKENED THAT THE VALVE CANNOT OPEN
FREELY
OBSTRUCTS THE NORMAL FLOW OF BLOOD
▪MITRAL
STENOSIS Add a Slide Title -
4
 DEFINITION

▪ Mitral stenosis is an obstruction to blood flowing from the

left atrium into the left ventricle.
▪ It most often is caused by rheumatic endocarditis, which
progressively thickens mitral valve leaflets and chordae
tendineae.
▪ Leaflets often fuse together. Eventually, the mitral valve
orifice narrows and progressively obstructs blood flow into
the ventricle.
ETIOLOGY

 Leading cause-Rheumatic fever, causing post-rheumatic deformities.

 Other rare aetiologies of left atrial outflow obstruction include
congenital and degenerative mitral valve stenosis, severe mitral
annular and/or leaflet calcification carcinoid disease, neoplasm, left
atrial thrombus, infective endocarditis with large vegetations,
 Certain inherited metabolic disorders such as fabry’s disease,
mucopolysaccharidosis, whipple ’s disease, gout, rheumatic arthritis,
lupus erythematosus, methysergide therapy
 Cases related to previous implanted prosthesis or commisurotomy.
 CLINICAL MANIFESTION
▪ Symptoms usually develop after the valve opening is reduced by one third to one half its
usual size.
▪ Dyspnea on exertion (DOE) as a result of pulmonary venous hypertension.
▪ Patients may experience progressive fatigue and decreased exercise tolerance as a result
of low cardiac output.
▪ An enlarged left atrium may create pressure on the left bronchial tree, resulting in a dry
cough or wheezing.
▪ Mitral face :(abnormal flushing of the cheeks that occurs from cutaneous vasodilation)
▪ Patients may expectorate blood (i.e., hemoptysis) or experience palpitations, orthopnea,
paroxysmal nocturnal dyspnea (PND), and repeated respiratory infections.
▪ As a result of increased blood volume and pressure, the atrium dilates, hypertrophies,
and becomes electrically unstable (patients experience atrial dysrhythmias).
ASSESSMENT AND DIAGNOSTIC EVALUATION

▪ History collection
▪ Physical examination
▪ Investigations like
a. ECG
b. Blood investigation
c. Echocardiography
d. X ray , CT , MRI .
e. Invasive diagnostic evaluation
MANAGEMENT

MEDICAL SURGICAL
▪ Anticoagulant ( to reduce the ▪ Mitral ballon vavuloplasty
risk of systemic embolism)
▪ Mitral valvotomy
▪ Digoxin, beta blockers,calcium
channel blockers( to control ▪ Valve replacement
ventricular rate in atrial
fibrillation)
▪ Diuretic( to control pulmonary
congestion)
▪AORTIC
STENOSIS
 DEFINITION

▪ Aortic valve stenosis is narrowing of the orifice between the left ventricle and aorta.
▪ In adults, stenosis often is a result of degenerative calcifications. Calcifications may be
caused by proliferative and inflammatory changes that occur in response to years of normal
mechanical stress, similar to changes that occur in atherosclerotic arterial disease.
▪ Diabetes, hypercholesterolemia, hypertension, and low levels of high-density lipoprotein
cholesterol may be risk factors for degenerative changes of the valve.
▪ Congenital leaflet malformations or an abnormal number of leaflets (i.e., one or two rather
than three) may be involved.
▪ Rheumatic endocarditis may cause adhesions or fusion of the commissures and valve ring,
stifening of the cusps, and calcific nodules on the cusps.
 CAUSES

▪ Age-related degenerative calcified aortic stenosis is the most common cause

of aortic stenosis in adults
▪ The second most common cause is calcification of a congenitally bicuspid
aortic valve.
▪ Other rare causes of calcified aortic stenosis include Fabry disease, lupus
erythematosus, Paget disease, and ochronosis with alkaptonuria.
▪ The most common etiology of aortic stenosis worldwide remains rheumatic
heart disease
PATHOPHYSIOLOGY
 Clinical manifestation
▪ Many patients with aortic stenosis are asymptomatic.
▪ When symptoms develop, patients usually first have exertional dyspnea, caused by
increased pulmonary venous pressure due to left ventricular failure.
▪ Orthopnea, PND, and pulmonary edema also may occur.
▪ Reduced blood flow to the brain may cause dizziness and syncope.
▪ Angina pectoris is a frequent symptom; it results from increased oxygen demand of the
hypertrophied left ventricle with decreased blood supply due to decreased blood flow into
the coronary arteries and decreased time in diastole for myocardial perfusion.
▪ Blood pressure is usually normal but may be low. Pulse pressure may be low (30 mmHg
or less) because of diminished blood flow.
 ASSESSMENT AND DIAGNOSTIC EVALUATION
▪ History collection
▪ Physical examination
i. Loud, rough systolic murmur may be heard over the aortic area and may radiate to the carotid
arteries and apex of the left ventricle. The murmur is low-pitched, crescendo–decrescendo,
rough, rasping, and vibrating.
ii. An S4 sound may be heard.
iii. If the examiner rests a hand over the base of the heart (second intercostal space next to the
sternum and above the suprasternal notch) and up along the carotid arteries, a vibration may be
felt. The vibration is caused by turbulent blood flow across the narrowed valve orifice.
iv. By having the patient lean forward during auscultation and palpation, especially during
exhalation, it is possible to accentuate sounds of aortic stenosis (Hogan-Quigley et al., 2012).
▪ Echocardiography, CMR imaging, and computed tomography (CT)
MANAGEMENT
MEDICAL
▪ Medications are prescribed to treat
dysrhythmia or left ventricular
failure
▪ Medications like Digoxin, beta
blockers,calcium channel blockers,
diuretics
▪ Na+ restriction,Reduced activity
SURGICAL
▪ surgical replacement of the aortic
valve. ( mechanical/biological )
▪ Percutaneous aortic ballon
valvuloplasty
▪ Transcatheter aortic valve
implantation (TAVI).
▪PULMONARY
STENOSIS
DEFINITION AND ETIOLOGY
▪ Stenosis is caused by fusion of the pulmonary valve leaflets and a narrowed
central orifice.
▪ Pulmonary valve stenosis can be caused congenital, carcinoid and rheumatic
disorders or extrinsic compression.
▪ The typical domeshaped pulmonary valve stenosis is the most common form of
right ventricular outflow tract obstruction..
▪ The valve is usually mobile and associated with medial abnormalities and dilation
of the pulmonary trunk.
▪ Pulmonary valve stenosis may be associated with Noonan, Williams, Alagille,
Keutel or rubella syndromes
CLINICAL MANIFESTATIONS

▪ Most patients with mild to moderate pulmonary valve stenosis are

asymptomatic.
▪ Severe pulmonary valve stenosis may cause
i. exertional dyspnea,
ii. fatigue,
iii. chest pain,
iv. palpitations and syncope.
ASSESSMENT AND DIAGNOSTIC EVALUATION

▪ History collection
▪ Physical examination-- thrill along the left sternal edge, and a long systolic
ejection murmur with late peak may be appreciated. S2 may be widely split
with reduced or absent P2.
▪ Diagnostics test like
▪ Electrocardiography
▪ blood investigations
▪ 2d echocardiograpy
▪ Cardiac catheterization
 MANAGEMENT

MEDICAL SURGICAL

▪ Supportive and symptomatic Balloon valvuloplasty.

treatment of right ventricular Pulmonary valve replacement
failure is recommended
▪TRICUSPID
STENOSIS
 DEFINITION AND CAUSES

▪ Usually occurs together with aortic or mitral stenosis

▪ May be due to rheumatic heart disease
▪ Tricuspid stenosis (TS) is most commonly of rheumatic origin and combined
with tricuspid regurgitation.
▪ The anatomical characteristics are similar to those of mitral stenosis, including
fibrous leaflet thickening and fusion and shortening of the subvalvular
apparatus.
▪ The preponderance of cases is in young women. Other aetiologies of right
atrial obstruction are rare and include congenital tricuspid atresia, right atrial
tumors and carcinoid syndrome
 CLINICAL MANIFESTATION

▪ Symptoms of right-sided heart failure

▪ Hepatomegaly
▪ Ascites
▪ Peripheral edema
▪ Neck vein engorgement
▪ fatigue, hypotension
 MANAGEMENT

MEDICAL SURGICAL

▪ Supportive and symptomatic Valve replacement

treatment Valvotomy
Balloon valvo plasty
Regurgitation
LEAKAGE OR BACKFLOW OF BLOOD
RESULTS FROM INCOMPLETE CLOSURE
OF THE VALVE
MITRAL VALVE
REGURGITATION
Add a Slide Title -
5
DEFINITION

▪ Mitral regurgitation involves blood flowing back from the

left ventricle into the left atrium during systole.
▪ Often, edges of mitral valve leaflets do not close completely
during systole because leaflets and chordae tendineae have
thickened and fibrosed, resulting in their contraction.
 ETIOLOGY

▪ The most common causes of mitral valve regurgitation in developed countries are degenerative
changes of the mitral valve (e.g., mitral valve prolapse) and ischemia of the left ventricle .
▪ The most common cause in developing countries is rheumatic heart disease and its sequelae
▪ .Other conditions that lead to mitral regurgitation include myxomatous changes, which enlarge and
stretch the left atrium and ventricle, causing leaflets and chordae tendineae to stretch or rupture.
▪ Infective endocarditis may cause perforation of a leaflet, or scarring following the infection may cause
retraction of leaflets or chordae tendineae.
▪ Collagen vascular diseases (e.g., systemic lupus erythematosus), cardiomyopathy, and ischemic heart
disease also may result in changes in the left ventricle, causing papillary muscles, chordae tendineae,
or leaflets to stretch, shorten, or rupture.
CLINICAL MANIFESTATION
SYMPTOMS
▪ Fatigue & weakness – due to 
CO – predominant complaint
▪ Exertional dyspnea & cough –
pulmonary congestion
▪ Palpitations – due to atrial
fibrillation (occur in 75% of pts.)
▪ Edema, ascites – Right-sided heart
failure
SIGNS
▪ Atrial fibrillation
▪ Cardiomegally
▪ Apical pansystolic murmur +/- thrill
▪ Soft S1, apical S3
▪ Signs of pulmonary venous congestion
(crepitations, pulmonary edema, effusions)
▪ Signs of pulmonary hypertension & right
heart failure
ASSESSMENT AND DIAGNOSTIC
EVALUATION

▪ History collection
▪ Physical examination-- A systolic murmur is a high-pitched, blowing
sound at the apex .
▪ The pulse may be regular and of good volume, or it may be irregular as
a result of extra systolic beats or atrial fibrillation.
▪ Echocardiography issused to diagnose and monitor the progression of
mitral regurgitation.
▪ Transesophageal echocardiography (TEE) provides the best images of
the mitralvalve.
MANAGEMENT
MEDICAL SURGICAL
▪ Angiotensin-converting enzyme (ACE) ▪ Mitral valvuloplasty (i.e., surgical
inhibitors such as captopril (capoten),
enalapril (vasotec), lisinopril (prinivil, zestril)
repair of the valve)
orramipril (altace), or hydralazine (apresoline)
▪ valve replacement
▪ Beta-blockers, such as carvedilol (coreg).
▪ Anticoagulants
▪ Digoxin
▪ Diuretics
▪ Restrict his or her activity level to minimize
symptoms.
▪Aortic valve
regurgitation
Definition and Etiology

▪ Aortic Regurgitation is flow of blood back into the left ventricle from
the aorta during diastole.
▪ It may be caused by inflammatory lesions that deform aortic valve
leaflets or dilation of the aorta, preventing complete closure of the
aortic valve.
▪ This valvular defect also may result from infective or rheumatic
endocarditis, congenital abnormalities, diseases such as syphilis, a
dissecting aneurysm that causes dilation or tearing of the ascending
aorta, blunt chest trauma, or deterioration of a surgically replaced
aortic valve.
 Clinical manifestation

Some patients are aware of a forceful heartbeat ( palpitation), especially in the head or neck
Marked arterial pulsations visible or palpable at carotid or temporal arteries may be present
as a result of increased force and volume of blood ejected from a hypertrophied left
ventricle.
Exertional dyspnea and fatigue
Signs and symptoms of progressive left ventricular failure include breathing difficulties
(e.g., orthopnea, PND).
pathophysiology
Incomplete closure of the
aortic valve

Blackflow of blood to
left ventricle

left ventricular hypertrophy &

Left atrial pressure
dilation

Left atrium hypertrophy

Left sided heart failure
(late stage)

Pulmonary hypertension
co2

Right ventricular pressure

Right sided heart failure
 Assessment and diagnostic evaluation

▪ History collection
▪ Physical assessment

Pulses
Large volume or ‘collapsing’ pulse
Low diastolic and increased pulse pressure
Bounding peripheral pulse
Capillary pulsation in nail beds: Quincke’s
sign
Femoral bruit(‘pistol shot’): Duroziez’s sign
Head nodding with pulse: de Musset’s sign
 MANAGEMENT
▪ Treatment may be required for underlying conditions, such as endocarditis
or syphilis
▪ Aortic regurgitation with symptoms aortic valve replacement (may be
combined with aortic root replacement and coronary bypass surgery)
▪ Asymptomatic patients annually follow up with echocardiography for
evidence of increasing ventricular size
▪ Systolic BP should be controlled with vasodilating drugs, such as
nifedipine or ACE inhibitors
▪PULMONIC VALVE
REGURGITATION
 DEFINITION AND ETIOLOGY

▪ Physiologic pulmonic regurgitation, qualified as trace to mild, is present in

nearly all individuals.
▪ Pulmonary valve regurgitation can be caused by valvular disease such as
infective endocarditis (rarely involves pulmonic valve) or connective tissue
disease, carcinoid, congenital heart disease, or it can be secondary to
pulmonary hypertension, which causes dilation of the valve ring.
▪ Pulmonic regurgitation can result in impairment of right ventricular function
and eventual clinical manifestations of right-sided volume overload and heart
failure.
 Clinical manifestation

▪ Symptoms of right-sided heart failure

▪ Dyspnea on exertion
▪ Light-headedness,
▪ Lethargy,
▪ Peripheral edema,
▪ Chest pain,
▪ Palpitations,
▪ Abdominal pain.
 Assesment and diagnostic evaluation
▪ History collection
▪ Physical examination—
i. A palpable impulse may be present at the left lower sternal border due to right
ventricular enlargement.
ii. On auscultation P2 may be delayed due to increased right ventricular end-
diastolic volume and increased ejection time with large stroke volume.
iii. The murmur of pulmonary regurgitation is heard best at the third to fourth
intercostal space along the left sternal border and increases with inspiration.
Investigations like ECG ,Blood investigations ,Echocardiography, X ray , CT ,
MRI ,Invasive diagnostic evaluation
 MANAGEMENT

▪ Treating the cause of pulmonary hypertension can relieve symptoms and

decrease the severity of PR If medical management is insufficient, surgical
treatment options should be evaluated.
▪ The presence of severe right heart failure due to pulmonic regurgitation
surgical pulmonic valve reconstruction or replacement can be considered.
▪TRICUSPID VALVE
REGURGITATION
 DEFINITION AND ETIOLOGY
Functional tricuspid regurgitation results from distortion of the architecture and coordinated actions of the
tricuspid leaflets, annulus, chords, papillary muscles, and right ventricular (RV) wall.

This distortion is most commonly caused by right ventricular dilation and dysfunction from left sided
heart disease with pressure/volume overload conditions.

Pure tricuspid regurgitation may result from rheumatic fever, infective endocarditis, carcinoid causes,
rheumatoid arthritis, radiation therapy, anorectic drugs, trauma, Marfan’s syndrome, tricuspid valve
prolapse, papillary muscle dysfunction, or congenital disorders.

Right ventricular infarction with severe regional wall motion abnormality or disruption of the papillary
muscle may cause regurgitation.

Right ventricular dilatation with annular enlargement and valvular incompetence can be seen in
Eisenmenger syndrome and pulmonary hypertension.
 CLINICAL MANIFESTATION

▪ A reduction in cardiac output related to tricuspid regurgitation, may cause

symptoms of fatigue and weakness.
▪ Right-sided heart failure may cause ascites, congestive hepatosplenomegaly,
pulsatile liver, pleural effusions, and peripheral edema.
ASSESSMENT AND DIAGNOSTIC EVALUATION

▪ History collection
▪ Physical examination With progression of the disease, patients become cachexic, cyanotic
and jaundice may be present.
▪ A parasternal pansytolic murmur increasing on inspiration may be appreciated on
auscultation(Carvallo’s sign).
▪ An S3, increasing with inspiration and decreasing with a Valsalva maneuver may be
audible, as well as an increased P2 if pulmonary hypertension has developed.
▪ Investigations like Chest Radiography, Echocardiography , Cardiac catheterization
MANAGEMENT

MEDICAL
▪ medical management alone may
minimize the need for surgical
intervention
SURGICAL
▪ Annuloplasty or valve replacement
with a mechanical valve or
bioprosthesis.
▪ Suture annuloplasty (de vega
procedure) or by ring annuloplasty.
▪ Bioprostheses are generally
preferred above mechanical
prostheses for the tricuspid position,
as mentioned in the section about
tricuspid stenosis.
Nursing
management
Based on the assessment data, major nursing diagnoses may include the
following:
▪ Decreased cardiac output related to structural disorders caused by cardiomyopathy or
to dysrhythmia from the disease process and medical treatments
▪ Risk for ineffective cardiac, cerebral, peripheral, and renal tissue perfusion related to
decreased peripheral blood flow (resulting from decreased cardiac output)
▪ Impaired gas exchange related to pulmonary congestion caused by myocardial failure
(resulting from decreased cardiac output)
▪ Activity intolerance related to decreased cardiac output or excessive fluid volume, or
both
▪ Anxiety related to the change in health status and in role functioning
▪ Powerlessness related to disease process • Noncompliance with medication and diet
therapies
 Decreased cardiac output related to structural disorders
caused by cardiomyopathy or to dysrhythmia from the
disease process and medical treatments

▪ Record intake and output. If patient is acutely ill, measure hourly urine output and note
decreases in output.
▪ For patients with increased preload, limit fluids and sodium as ordered.
▪ Closely monitor fluid intake including IV lines. Maintain fluid restriction if ordered.
▪ Auscultate heart sounds; note rate, rhythm, presence of S3, S4, and lung sounds.
▪ Closely monitor for symptoms of heart failure and decreased cardiac output, including
diminished quality of peripheral pulses, cold and clammy skin and extremities, increased
respiratory rate, presence of paroxysmal nocturnal dyspnea or orthopnea, increased heart
rate, neck vein distention, decreased level of consciousness, and presence of edema.
▪ Note chest pain. Identify location, radiation, severity, quality, duration, associated
manifestations such as nausea, and precipitating and relieving factors.
▪ If chest pain is present, have patient lie down, monitor cardiac rhythm, give oxygen, run a
strip, medicate for pain, and notify the physician.
▪ Place on cardiac monitor; monitor for dysrhythmias, especially atrial fibrillation.
▪ Examine laboratory data, especially arterial blood gases and electrolytes, including potassium,
complete blood count, sodium level, and serum creatinine.
▪ Administer medications as prescribed, noting side effects and toxicity.
▪ Review results of EKG and chest Xray.
▪ Position patient in semi-Fowler’s to high-Fowler’s
▪ Administer oxygen therapy as prescribed.
▪ During acute events, ensure patient remains on bed rest or maintains activity level that does not
compromise cardiac output.
▪ Monitor bowel function. Provide stool softeners as ordered. Tell patient to avoid straining when
defecating.
▪ Monitor blood pressure, pulse, and condition before administering cardiac medications such as
angiotensin converting enzyme (ACE) inhibitors, digoxin, and beta-blockers such as carvedilol.
Notify physician if heart rate or blood pressure is low before holding medications.
 OTHER MAJOR INTERVENTIONS INCLUDE

▪ Improving Cardiac Output and Peripheral Blood Flow

▪ Increasing Activity Tolerance and Improving Gas Exchange
▪ Reducing Anxiety
▪ Decreasing The Sense Of Powerlessness
▪ Promoting Home and Community-Based Care