Valvular heart disease

1. MEDICAL NURSING 1
VALVULAR HEART DISEASE
 GROUP MEMBERS
 NABIBYE MIRIA
 ENSITERIYEITU JANUARIO

2. INTRODUCTION
 Valvular heart disease is characterized by narrowing or leaking of
any of those or more valve.
 There are four heart valves that is mitral valve, pulmonic valve, aortic
valve and tricuspid valve.
 These control the flow of blood through the heart into the
pulmonary artery and aorta by opening and closing in response to
the blood pressure changes as the heart contracts and relaxes
through out the cardiac cycle.

3. Cont…

4. LOCATION OF THE VALVES
 Atrioventricular valves :tricuspid valve (three leaflets) which separates the
right atrium from the right ventricle and the mitral valve (two leaflets)
which separates the left atrium from the left ventricle
 Both valves have chordae tendineae that anchor the valve leaflets to the
papillary muscles and ventricular wall.
 Semilunar valves : pulmonic lies between the right ventricle and the
pulmonary artery and aortic valves which lies between the left ventricle
and the aorta.
NB: When valves do not close completely, regurgitation occurs and when
the valves do not open completely, it leads to stenosis that is to say the
flow of blood through the valve is reduced

5. Epidemiology of valvular heart diseases
 The VHD incidence rises with age
 Data from population studies points to a prevalence of 13.3% in 75yrs and
older group.
 Prevalence of moderate or severe valvular disease is 1.8% on basis of
symptoms or cardiac murmur auscultation cc is in contrast with 2.5%
determined by echocardiographic findings that shows that the burden of
VHD is underestimated when assessed by clinical data
 Degeneretative diseases account for 63% of all the VHD then RF accounts
for 22%.

6. Cont..
 In SA, RF accounted for 72% of the VHD and 68% were women of median
age of 43 yrs
 In a survey in Turkish, a median age of 57yrs accounts for 60% 0f VHD
among women.

7. CAUSES
 RHD, the most common cause
 Infective endocarditis
 Non bacterial thrombotic endocarditis
 Syphilitic valvulitis
 Calcific stenosis
 Myomatous degeneration
 Carcinoid heart disease

8. CLASSIFICATION OR TYPES OF VALVULAR
DISEASE
1. Valvular Stenosis:
 Results from a narrowing of the valve orifice that is usually caused by a
thickening and increased rigidity of the valve leaflets. The narrowed opening
may make the heart work very hard to pump blood through it.
 All four valves can be stenosis such as- Aortic stenosis, Mitral Stenosis, Tricuspid
Stenosis, Pulmonic Stenosis.
2. Valvular Insufficiency:
 Results from the valve leaflets not completely sealing when the valve is closed so
that a backward flow (Regurgitation) of blood occurs into the heart.
 Depending on which valve is affected, the condition is called tricuspid
regurgitation, pulmonary regurgitation, mitral regurgitation or aortic
regurgitation.

9. MITRAL VALVE PROLAPSE
 Mitral valve prolapse, formerly known as mitral prolapse syndrome, is a
deformity that usually produces no symptoms.
 Rarely, it progresses and can result in sudden death.
 Mitral valve prolapse occurs more frequently in women than in men.

10. pathophysiology
 In mitral valve prolapse, a portion of a mitral valve leaflet balloons back
into the atrium during systole.
 Rarely, the ballooning stretches the leaflet to the point that the valve does
not remain closed during systole ( ventricular contraction).
 Blood then regurgitates from the left ventricle back into the left atrium

11. Risk factors
 Marfan syndrome ( genetic disease of connective tissue)
 Ehlers-Danlos syndrome ( genetic disease that weakens connective tissue)
 Muscular dystrophy ( a group of diseases that cause progressive weakness
and loss of muscle mass)

12. Assessment and Diagnostic Findings
 Physical examination of the heart discloses an extra heart sound, referred
to as a mitral click.
 The systolic click is an early sign that a valve leaflet is ballooning into the
left atrium.
 In addition to the mitral click, a murmur of mitral regurgitation may be
heard if progressive valve leaflet stretching and regurgitation have
occurred.

13. Clinical manifestation
 Many people have a ballooned leaflet but no symptoms.
 Fatigue, light-headedness, dizziness, syncope, palpitations, and anxiety,
 Fatigue may occur regardless of the person’s activity level and amount of
rest or sleep.
 Shortness of breath, atrial or ventricular dysrhythmias may produce the
sensation of palpitations, chest pain.

14. complications
 Mitral valve regurgitation. The most common complication is a condition
in which the valve leaks blood back into the left atrium (mitral valve
regurgitation)
 Heart rhythm problems (arrhythmias)
 Heart valve infection (endocarditis)

15. Medical management
 If dysrhythmias are documented and cause symptoms, the patient is
advised to eliminate caffeine and alcohol from the diet and to stop
smoking; anti arrhythmic medications may be prescribed.
 Chest pain that does not respond to nitrates may respond to calcium
channel blockers or beta-blockers.
 Heart failure is treated the same as it would be for any other patient with
heart failure.
 mitral valve repair or replacement may be necessary.

16. Nursing management
 Educate patients about the diagnosis and the possibility that the condition is
hereditary.
 Explain the need to inform the health care provider about any symptoms that
may develop.
 The nurse also instructs patients about the need for prophylactic antibiotic
therapy before undergoing invasive procedures (eg, dental work, genitourinary
or gastrointestinal procedures) that may introduce infectious agents system.
 This therapy is prescribed for symptomatic patients and for asymptomatic
patients who have both a systolic click and murmur or mitral regurgitation. If in
doubt about risk factors and the need for antibiotics, patients should consult
their physicians

17. Cont….
 The nurse teaches patients to avoid caffeine and alcohol.
 The nurse encourages patients to read product labels, particularly in over-
the-counter products such as cough medicine, because these products
may contain alcohol, caffeine, ephedrine, and epinephrine, which may
produce dysrhythmias and other symptoms.
 Dysrhythmias, chest pain, heart failure, or other complications of mitral
valve prolapse are treated.
 The nurse also explores with patients possible diet, activity, sleep, and
other lifestyle factors that may correlate with symptoms experienced

18. Nursing care plan
DIAGNOSES
 Anxiety related to fear of heart disease and implications for lifesty
 Risk of infection (endocarditis) related to altered valve function
EXPECTED OUTCOMES
 Verbalize an understanding of MVP and its management.
 Discuss ways to decrease or relieve MVP symptoms.
 Acknowledge the risk for endocarditis and identify precautions to prevent it.
PLANNING AND IMPLEMENTATION
 Consult with and refer to cardiologist for continued monitoring and follow-up.
 Teach about MVP, including heart valve anatomy, physiology, and function, common
manifestations of MVP, and treatment rationale.
 Discuss symptoms of progressive mitral regurgitation, and the need to report these to
the cardiologist.

19. CONT…
 Discuss recommended follow-up care and its rationale.
 Allow to verbalize feelings and share concerns about MVP. Encourage to
attend an MVP support group meeting.
 Discuss the prognosis for MVP, emphasizing that most clients live normal
lives using diet and lifestyle management.
 Instruct to keep a weekly record of symptoms and their frequency for 1
month.

20. Cont..
 Discuss lifestyle changes to manage symptoms: aerobic exercise with
warm up and cooled own periods; maintaining adequate fluid intake,
especially during hot weather or exercise; relaxation techniques (e.g.,
meditation, deep-breathing exercises, music therapy, yoga, guided
imagery, heat therapy, or progressive muscle relaxation) to perform daily;
avoiding caffeine and crash diets; forming healthy eating habits.
 Teach about infective endocarditis risk and prevention with prophylactic
antibiotics. Encourage notifying dentist and other health care providers of
MVP before dental or any invasive procedure

21. Evaluation
 verbalizes an understanding of MVP by explaining heart valve function,
listing common manifestations of MVP, and describing indications of
deteriorating heart function.
 verbalizes understanding of the risk of endocarditis, and states that she
will notify her doctors of her MVP and the need for antibiotics before
invasive procedures
 moderated her caffeine intake and increased her fluids, relieving her
symptoms.
 taking a relaxation music therapy class

22. MITRAL REGURGITATION
 Mitral regurgitation involves blood flowing back from the left ventricle
into the left atrium during systole.
 Often, the margins of the mitral valve cannot close during systole.
 Causes
 mitral valve prolapse, damaged tissue cords, RF, endocarditis, heart
attack, abnormality of the heart muscle, trauma, congenital heart defects,
radiation therapy but very rare

23. Risk factors
 Heart attack
 Heart disease such as coronary artery disease
 A history of mitral valve prolapse or mitral valve stenosis
 Infections such as endocarditis or rheumatic fever
 Congenital heart disease
 Age (middle age)

24. pathophysiology
 Mitral regurgitation may be caused by problems with one or more of the
leaflets, the chordae tendineae, the annulus, or the papillary muscles.
 A mitral valve leaflet may shorten or tear.
 The chordae tendineae may elongate, shorten, or tear.
 The annulus may be stretched by heart enlargement or deformed by
calcification.
 The papillary muscle may rupture, stretch, or be pulled out of position by
changes in the ventricular wall (eg, scar from a myocardial infarction or
ventricular dilation).

25. CONT.
 The papillary muscle may be unable to contract because of ischemia.
 With each beat of the left ventricle, some of the blood is forced back into the
left atrium.
 Because this blood is added to the blood that is beginning to flow in from the
lungs, the left atrium must stretch.
 It eventually hypertrophies and dilates.
 The backward flow of blood from the ventricle diminishes the volume of blood
flowing into the atrium from the lungs.
 As a result, the lungs become congested, eventually adding extra strain on the
right ventricle.
 Mitral regurgitation ultimately involves the lungs and the right ventricle.
Clinical Manifest

26. Clinical Manifestations
 Chronic mitral regurgitation is often asymptomatic.
 Acute mitral regurgitation (eg, that resulting from a myocardial
infarction) usually manifests as severe congestive heart failure.
 Dyspnea, fatigue, and weakness are the most common symptoms.
 Palpitations, shortness of breath on exertion, and cough from pulmonary
congestion also occur

27. complication
 Heart failure
 Aortic fibrillation ( irregular heart rhythm x-terised by very rapid and
chaotic atrial contractions)
 Pulmonary hypertension

28. Assessment and diagnostic findings
 A systolic murmur is heard as 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 extrasystolic beats or Atrial fibrillation.
 Echocardiography is used to diagnose and monitor the progression of
mitral regurgitation

29. Medical management
 Management of mitral regurgitation is the same as that for congestive
heart failure.
 Surgical intervention consists of mitral valve replacement or valvuloplasty
(ie, surgical repair of the heart valve).

30. Nursing care plan
 Activity intolerance ;related to imbalanced oxygen supply and demand due to heart
chambers not fully filling due to valve allowing back flow of red blood cells carrying
oxygen to not reach the body systematically.
 Evidenced: by a patient complaining of difficulty in breathing when performing simple
tasks, patient having difficulties of performing activities of daily living, easy fatigability,
limitation in activities.
 Goals: patient will be able to move from lying down position to siting position without
getting light headedness at the end of the day, patient will be able to do activities of
daily living without difficulty in breathing by the end of the week
 Have the patient perform activity more slowly : this helps in increasing for activity
tolerance: patient well tolerated the activity of moving from lying to sitting position.
 Monitor physiological responses to increase the activity like respirations, SPO2, HR and
BP: values should return normal with in 5 min or less: patient expresses satisfaction
with increase in the activity level, BP, HR, SPO2 remained stable at the end of the
activity.

31. Mitral stenosis
 Mitral stenosis is an obstruction of blood flowing from the left atrium into
the left ventricle.
 It is most often caused by rheumatic endocarditis, which progressively
thickens the mitral valve leaflets and chordae tendineae.
 The leaflets often fuse together.
 Eventually, the mitral valve orifice narrows and progressively obstructs
blood flow into the ventricle.

32. cause
 Congenital heart defects
 Calcium build up on the valve
 Rheumatic fever
 Risks
 Older age
 Certain heart conditions present at birth (congenital heart disease) such
as a bicuspid aortic valve, History of infections that can affect the heart
 Having cardiovascular risk factors, such as diabetes, high cholesterol and
high blood pressure, Chronic kidney disease, History of radiation therapy
to the chest

33. pathophysiology
 Normally, the mitral valve opening is as wide as the diameter of three fingers.
 In cases of marked stenosis, the opening narrows to the width of a pencil.
 The left atrium has great difficulty moving blood into the ventricle because of
the increased resistance of the narrowed orifice; it dilates (stretches) and
hypertrophies (thickens) because of the increased blood volume it holds.
 Because there is no valve to protect the pulmonary veins from the backward flow
of blood from the atrium, the pulmonary circulation becomes congested.
 As a result, the right ventricle must contract against an abnormally high
pulmonary arterial pressure and is subjected to excessive strain. Eventually, the
right ventricle fails

34. Clinical manifestation
 The first symptom of mitral stenosis is often breathing difficulty (ie,
dyspnea) on exertion as a result of pulmonary venous hypertension.
 Patients with mitral stenosis are likely to show progressive fatigue as a
result of low cardiac output.
 They may expectorate blood (ie, hemoptysis), cough, and experience
repeated respiratory infections.

35. Assessment and diagnostic findings
 The pulse is weak and often irregular because of atrial fibrillation (caused
by the strain on the atrium).
 A low-pitched, rumbling, diastolic murmur is heard at the apex.
 As a result of the increased blood volume and pressure, the atrium dilates,
hypertrophies, and becomes electrically unstable, and the patient
experiences atrial dysrhythmias.
 Echocardiography is used to diagnose mitral stenosis.
Electrocardiography (ECG) and cardiac catheterization with angiography
are used to determine the severity of the mitral stenosis

36. complications
 Heart failure
 Stroke
 Blood clots
 Bleeding
 Heart rhythm abnormalities (arrhythmias)
 Infections that affect the heart, such as endocarditis

37. Medical management
 Antibiotic prophylaxis therapy is instituted to prevent recurrence of
infections.
 Congestive heart failure is treated.
 Patients with mitral stenosis may benefit from anticoagulants to decrease
the risk for developing Atrial thrombus.
 They may also require treatment for anemia.
 Surgical intervention consists of valvuloplasty, usually a commissurotomy
to open or rupture the fused commissures of the mitral valve.
 Percutaneous transluminal valvuloplasty or mitral valve replacement may
be performed

38. prevention
 Taking steps to prevent rheumatic fever
 Addressing risk factors for coronary artery disease
 Taking care of your teeth and gums

39. AORTIC REGURGITATION
 Aortic regurgitation is the flow of blood back into the left ventricle from
the aorta during diastole.
 It may be caused by inflammatory lesions that deform the leaflets of the
aortic valve, preventing them from completely closing the aortic valve
orifice.
 This valvular defect also may result from endocarditis, congenital
abnormalities, diseases such as syphilis, a dissecting aneurysm that causes
dilation or tearing of the ascending aorta, or deterioration of an aortic
valve replacement.

40. CAUSES
 Congenital heart valve disease. You may have been born with an aortic
valve that has only two cusps (bicuspid valve) or fused cusps rather than
the normal three separate cusps. In some cases a valve may only have one
cusp (unicuspid) or four cusps (quadricuspid), but this is less common.
 Age-related changes to the heart. Calcium deposits can build up on the
aortic valve over time, causing the aortic valve's cusps to stiffen. This can
cause the aortic valve to become narrow, and it may also not close
properly.
 Endocarditis. The aortic valve may be damaged by endocarditis — an
infection inside your heart that involves heart valves.

41. CAUSES
 Rheumatic fever. Rheumatic fever — a complication of strep throat and
once a common childhood illness can damage the aortic valve.
 Other diseases. Other rare conditions can enlarge the aorta and aortic
valve and lead to regurgitation, including Marfan syndrome, a connective
tissue disease. Some autoimmune conditions, such as lupus, also can lead
to aortic valve regurgitation.
 Trauma. Damage to the aorta near the site of the aortic valve, such as
damage from injury to your chest or from a tear in the aorta, also can cause
backward flow of blood through the valve

42. RISK FACTORS
 Older age
 Certain heart conditions present at birth (congenital heart disease)
 History of infections that can affect the heart
 Certain conditions that can affect the heart, such as Marfan syndrome
 Other heart valve conditions, such as aortic valve stenosis
 High blood pressure
 Obesity

43. pathophysiology
 In aortic regurgitation, blood from the aorta returns to the left ventricle
during diastole in addition to the blood normally delivered by the left
atrium.
 The left ventricle dilates, trying to accommodate the increased volume of
blood. It also hypertrophies, trying to increase muscle strength to expel
more blood with above normal force—raising systolic blood pressure.
 The arteries attempt to compensate for the higher pressures by reflex
vasodilation; the peripheral arterioles relax, reducing peripheral
resistance and diastolic blood pressure.

44. Clinical manifestation
 Aortic insufficiency develops without symptoms in most patients. Some
patients are aware of a forceful heartbeat, especially in the head or neck.
 There may be marked arterial pulsations that are visible or palpable at the
carotid or temporal arteries.
 This is a result of the increased force and volume of the blood ejected
from the hypertrophied left ventricle. Exertional dyspnea and fatigue
follow.
 Progressive signs and symptoms of left ventricular failure include
breathing difficulties (eg, orthopnea, paroxysmal nocturnal dyspnea),
especially at night.

45. COMPLICATIONS
 Heart failure
 Infections that affect the heart, such as endocarditis
 Heart rhythm abnormalities

46. Assessment and diagnostic findings
 A diastolic murmur is heard as a high-pitched, blowing sound at the third
or fourth intercostal space at the left sternal border.
 The pulse pressure (ie difference between systolic and diastolic pressures)
is considerably widened in patients with aortic regurgitation.
 water-hammer pulse, in which the pulse strikes the palpating finger with a
quick, sharp stroke and then suddenly collapses.
 Diagnosis may be confirmed by echocardiogram, radionuclide imaging,
ECG, magnetic resonance imaging, and cardiac catheterization.

47. Medical management
 Before the patient undergoes invasive or dental procedures, antibiotic
prophylaxis is needed to prevent endocarditis.
 Heart failure and dysrhythmias are treated.
 Aortic valvuloplasty or valve replacement is the treatment of choice,
preferably performed before left ventricular failure.
 Surgery is recommended for any patient with left ventricular hypertrophy,
regardless of the presence or absence of symptoms.

48. AORTIC STENOSIS
 Aortic valve stenosis is narrowing of the orifice between the left ventricle
and the aorta.
causes
 congenital leaflet malformations or an abnormal number of leaflets (ie,
one or two rather than three)
 rheumatic endocarditis or cusp calcification of unknown cause.
 The leaflets of the aortic valve may fuse

49. pathophysiology
 There is progressive narrowing of the valve orifice, usually over a period of
several years to several decades.
 The left ventricle overcomes the obstruction to circulation by contracting
more slowly but with greater energy than normal, forcibly squeezing the
blood through the very small orifice.
 The obstruction to left ventricular outflow increases pressure on the left
ventricle, which results in thickening of the muscle wall. The heart muscle
hypertrophies.
 When these compensatory mechanisms of the heart begin to fail, clinical
signs and symptoms develop

50. Risk factors
 Old age
 Obesity
 Infections that affect the heart
 Diabetes, high cholesterol levels
 High blood pressure

51. Clinical manifestation
 Many patients with aortic stenosis are asymptomatic.
 Exertional Dyspnea, caused by left ventricular failure.
 Dizziness and syncope because of reduced blood flow to the brain.
 Angina pectoris is a frequent symptom that results from the increased
oxygen demands of the hypertrophied left ventricle, the decreased time in
diastole for myocardial perfusion, and the decreased blood flow into the
coronary arteries.
 Blood pressure can be low but is usually normal; there may be a low pulse
pressure (30 mm Hg or less) because of diminished blood flow.

52. Assessment and diagnostic findings
 On physical examination, a loud, rough systolic murmur may be heard
over the aortic area.
 The sound to listen for is a systolic crescendo-decrescendo murmur, which
may radiate into the carotid arteries and to the apex of the left ventricle.
 The murmur is low-pitched, rough, rasping, and vibrating. If the examiner
rests a hand over the base of the heart, a vibration may be felt.

53. CONT.
 The vibration is caused by turbulent blood flow across the narrowed valve
orifice. Evidence of left ventricular hypertrophy may be seen on a 12-lead
ECG and echocardiogram.
 Echocardiography is used to diagnose and monitor the progression of
aortic stenosis. After the stenosis progresses to the point that surgical
intervention is considered, left-sided heart catheterization is necessary to
measure the severity of the valvular abnormality and evaluate the
coronary arteries.
 Pressure tracings are taken from the left ventricle and the base of the
aorta. The systolic pressure in the left ventricle is considerably higher than
that in the aorta during systole.

54. COMPLICTIONS
 Heart failure.
 Stroke.
 Blood clots.
 Bleeding.
 Heart rhythm abnormalities (arrhythmias)
 Infections that affect the heart, such as endocarditis.

55. Medical management
 Antibiotic prophylaxis to prevent endocarditis is essential for anyone with
aortic stenosis.
 After left ventricular failure or dysrhythmias occur, medications are
prescribed.
 Definitive treatment for aortic stenosis is surgical replacement of the
aortic valve.
 Patients who are symptomatic and are not surgical candidates may benefit
from one- or two-balloon percutaneous valvuloplasty procedures

56. NURSING DIAGNOSIS OF VALVULAR HEART
DISORDERS
 Activity intolerance related to insufficient oxygenation secondary to
decreased cardiac output and pulmonary congestion difficult in breathing
when performing task, inability to do activities of daily living
Assess response to increased activity and help patient in daily activities.
 Deficient knowledge about self-care activities related to disease
manifestation, new diagnosis evidenced by patient verbalizing.
Explain drug regimen, purpose, dose, and side effects.
 Impaired gas exchange related to trauma of extensive chest surgery
evidenced by cyanosis
Administer O2 as ordered.

57. CONT.
 Decreased cardiac output related to blood loss and compromised
myocardial function evidenced by weak pulse, dizziness
 Anxiety related to threat of loss / death, Situational crisis, threats to self-
concept (self-image) evidenced by restlessness, tachypnea, too much
sweating, increased heart beat rate.
Maintain physical and emotional rest
Carefully maintain intake output and daily check weight.
 Ineffective Tissue perfusion related to decrease in peripheral blood
circulation, Cessation of arterial-venous flow, decrease in activity
evidenced by cold extremities, SPO2 reduced, poor skin turgor

58. CONT.
 Risk for ineffective renal perfusion related to decreased cardiac output,
hemolysis, or vasopressor drug therapy
 Risk for ineffective peripheral tissue perfusion related to decreased cardiac
output
 Risk for Fluid Volume Excess related to the displacement of the pressure on the
congestive pulmonary vein, decrease in perfusion organ (kidney); Increased
retention of sodium / water; Increased hydrostatic pressure, or decreased
plasma protein (absorbs liquid in the interstitial area / tissue).
 Carefully maintain intake output and daily check weight.
 Risk for Fluid Volume Deficit related to, decrease in cardiac output, decline in
glomerular filtration.
 Carefully maintain intake output and daily check weight.

59. NURSING INTERVENTIONS FOR VALVULAR
HEART DISEASE
 Assess mental status (Restlessness, severe anxiety and confusion).
 Check vital signs (heart rate and blood pressure).
 Assess heart sounds, noting gallops, S3, S4.
 Assess manually peripheral pulses (with weak rate, rhythm indicated low
cardiac output).
 Assess lung sounds and determine any occurrence of Paroxysmal Nocturnal
Dyspnea (PND) or othopnea.
 Monitor central venous, right arterial pressure [RAP], pulmonary arterial
pressure(PAP)
 Routinely Assess skin color and temperature (Cold, clammy skin is secondary to
compensatory increase in sympathetic nervous system stimulation and low
cardiac output and desaturation).

60. CONT.
 Administer medication as prescribed, noting response and watching for
side effects and toxicity.
 Administer stool softeners as needed(s training for a bowel movement
further impairs cardiac output).
 Maintain adequate ventilation and perfusion (Place patient in semi- to
high-Fowler’s position or supine position).
 Administer O2 as ordered.
 Explain diet restrictions (fluid, sodium).

61. OUTCOMES
 Normal blood circulation
 Reduced anxiety
 Normal fluid volume
 Patient verbalizing knowledge about self care
 Improved gaseous exchange
 Adequate tissue perfusion
 Normal urine output

62. PREVENTION
 Stop smoking.
 Consume no more than two alcoholic beverages a day.
 Eat a healthy, balanced diet (low salt and fat).
 Regular exercise and control weight.
 Maintain careful control of blood sugar.