Lecture no.4.cvs,h spptx CVS

LECTURE №4. The syndrome affection of the
heart valves.
Mitral stenosis. Mitral regurgitation.
Tricuspid stenosis. Tricuspid
regurgitation. Aortic stenosis. Aortic
regurgitation.
1

Cardiac Physiology 101
Systole AV/PV – opens
S1-S2 MV/TV – closes
Diastole AV/PV – closes
S2-S1 MV/TV – opens
2

Cardiac Physiology 101
Regurg/ Insuff – leaking (backflow) of blood across a closed valve
Stenosis – Obstruction of (forward) flow across an opened valve
Systole AV/PV – opens-------Aortic Stenosis
S1-S2 MV/TV – closes------Mitral Regurg
Diastole AV/PV – closes------Aortic Regurg
S2-S1 MV/TV – opens-------Mitral Stenosis
These concepts are set in stone, it can’t occur any other way,
It would be anatomically impossible
3

Aortic Stenosis
Etiologies
• Congenital 0-30 yrs
• Bicuspid 30-50 yrs
• Rheumatic 30-60 yrs
• Degenerative >60 yrs
6

Aortic Stenosis – pathophysiology
8

Aortic Stenosis – pathophysiology
9

Aortic Stenosis
Symptoms
• Angina
• Syncope
• Congestive Heart Failure (CHF)
10

Aortic Stenosis
Diagnosis
– Ecg – LAE, LVH
– Echo 2D/color doppler –test of choice
– Cardiac Cath – helpful, confirmatory, needed if
the pt is older – look at the coronaries
13

Aortic Stenosis
Treatment of Symptomatic Aortic Stenosis or
Decreased LV Function
Medical Therapy – treats the symptoms not the cause
Aortic Valve Replacement
Bioprosthetic vs Mechanical AVR
14

Valvular Heart Disease
Aortic Valve
• Aortic Stenosis
• Aortic Regurgitation
15

Aortic Regurgitation
Etiologies
• Abnormalities of the Leaflets
• Rheumatic, Bicuspid, Degenerative
• Endocarditis
• Dilation of the Aortic Annulus
• Aortic Aneurysm / Dissection
• Inflammatory (Syphyllis, Giant Cell Arteritis. Coll
Vasc Dis-Ankylosis Spondylitis, Reiters)
• Inheritable (Marfans, Osteogensis Imperfecta)
17

Aortic Regurg – pathophysiology
19

20

21

Physical Exam
• Diastolic Decrescendo Blowing Murmur
• Hyperdynamic LV apical impulse
• Bounding Pulses
• S4, S3 Gallop-advanced AI
• Apical Rumble – “Austin Flint Murmur”
23

Aortic Regurg – Austin Flint Murmur
Due to the vibration of the anterior leaflet of the mitral valve as it
is buffetted simultaneously by the blood jets from the left atrium
and the aorta.
24

Diagnosis
25

Treatment of Asymptomatic Aortic Regurg
• Serial Check ups with Echos (eval EF, Severity AR)
• SBE Prophylaxis
• Vasodialators (Nifedipine, ACE-I)
• Diuretics
Treatment of Symptomatic Aortic Regurg
Aortic Valve Replacement
Bioprosthetic vs Mechanical AVR
26

If you're not confused,
you're not paying
attention.
Tom Peters
27

Mitral Valve
• Mitral Regurgitation
• Mitral Stenosis
28

Mitral Regurgitation
Etiologies
• Alterations of the Leaflets, Commissures, Annulus
• Rheumatic
• MVP
• Endocarditis
• Alterations of LV or LA size and Function
• Papillary Muscle (Ischemic, MI, Myocarditis, DCM)
• HOCM
• LV Enlargement – Cardiomyopathies -
• LA Enlargement from MR –
– MR begets MR
29

Mitral Regurg – pathophysiology
31

32

33

Symptoms
• Fatigue and weakness
• Dyspnea and orthopnea
• Right sided HF
• MVP Syndrome (if present)
34

Physical Exam
• Holosystolic Apical Blowing Murmur
• Laterally displaced apical impulse
• Split S2 (but is obscured by the murmur)
• S3 Gallop (increased volume during diastole)
• Radiation depends on the etiology
35

Diagnosis
36

- SBE Prophylaxis
37

Mitral Regurgitation –MVP
Pathophysiology
40

Mitral Regurgitation -MVP
Diagnosis and Treatment
• Echo 2D/Color
• B-Blockers (hyperadrenergic symptoms, Palpitations)
• Aspirin (TIAs without etiology)
• SBE Prophylaxis (only if associated with MR)
• Severe Symptomatic MR – same as chronic MR
44

Mitral Valve
• Mitral Regurgitation
• Mitral Stenosis
45

Mitral Stenosis
Etiologies
• Rheumatic – almost all cases in adults
• Mitral Annular Ca+ - massive (rare)
• Congenital – rare
60% of pts don’t have a history of ARC
50% of pts who have ARC don’t develop VHD
46

Mitral Stenosis
Physical Exam
– Loud S1
– Opening Snap
– Diastolic Apical Rumble (murmur)
– May be associated with:
• MR or AS
• Right Sided Murmurs
o PI – Graham Steel Murmur
o TR
52

Mitral Stenosis
Diagnosis
– Ecg – A Fib, LAE, RAE, RVH
53

Mitral Stenosis
Treatment of Symptomatic Mitral Stenosis
• Diuretics – for congestion
• Digoxin, Beta and Ca Channel Blockers for Afib
rate control
• Anticoagulation – for AFib and LA clots
• SBE Prophylaxix – prevent endocarditis
54

Mitral Stenosis
Surgical Therapy – treats the cause
• Percutaneous Ballon Valvulaoplasty – Non-
calcified, pliable valve
55

Mitral Stenosis
Surgical Therapy – treats the cause
• Open Commisurotomy – valve repair
• Mitral Valve Replacement
56

Spectrum of VHD for Boards
Classic Areas boards will focus on – Physical Exams
Aotric Stenosis -severe
Aortic Regurg – Acute and Chronic
Mitral Stenosis
MVP – changes in MR with manuvers
IHSS/HOCM – changes in MR with manuvers
Mitral Regurg – Acute or chronic typically
associated with CAD or Ischemic HD
57

Aortic Stenosis
Physical Exam
• Harsh Systolic Ejection Murmur – late peaking
• S4 gallop (from LVH)
• Sustained Bifid LV impulse (from LVH)
• Pulsus Parvus et Tardus (Carotid Impulse)
58

Mitral stenosis
• Obstacle to a bloodflow from the left atrium
to the left ventricule, caused by narrowing left
atrio-ventricular apertures.
• The causes: the causes at adults practically
always is earlier transferred rheumatic fever.
Children with congenital mitral stenosis
seldom live more than 2th years. The causes
of obstruction left АV apertures can be and
micsoma the left atrium.
59

• Complaints: at early stages the mitral stenosis usually there
is a dyspnea at physical activity and fatigue. At the
moderate and severe stage the dyspnea disturbs even in
rest, palpitation, cough, hemoptysis, hypostases of feet.
The fever, a tachycardia at physical activity or atrial
fibrillation shortens time diastolic fillings of ventricules, the
insufficient bloodflow through narrowed left АV aperture
in a diasdolic phase promotes increase of pressure in the
left atrium and to reduction of cardiac output.
• Sudden increase of pressure in the left atrium conducts to
the expressed hypostasis of lungs. Hemoptysis, caused by
rupture of small pulmonary vessels, and also a hypostasis of
lungs, it is especially probable at pregnant women that is
connected with increase in volume of blood. The dilations
left atrium and the expanded pulmonary trunk can press
the left returnable nerve, cause its paralysis and hoarse
voices.
73

Survey:
• Acrocyonosis, «mitral face» - dark-violet colouring of cheekbones
against a pale skin (is more characteristic for patients with low
cardiac output and a high pulmonary hypertensia). There can be a
backlog in physical development, presence of "a cardiac hump» at
defect formation in the early childhood.
Palpation:
• On heart apex - diastolic trembling «the cat's purring», apex beat
more often it is not changed, in left parasternal areas - the
expressed pathological pulsation connected with a hypertrophy and
dilatation of right ventricule. In some cases are palpated I tone on
an apex of heart and click of opening of the mitral valve at a left
edge of the inferior part of a breast.
Percussion:
• The upper and right borders of relative dullness of heart are
displaced accordingly upwards and to the right.
74

Auscultation:
• On an apex it is audible loud hight I sound, or
«tone of closing» of the mitral valve. In
position of the patient on left to a side over
area where it is palpated apex beat, it is
listened rolling diastolic noise, usually with
presystolic murmur (if at the patient remains
the sinus rhythm). Accent II tone over a
pulmonary artery, additional tone «tone of
opening the mitral valve» at a left edge of the
inferior part of a breast; often heard the
tachysystolic form of atrial fibrillation.
75

Laboratory and instrumental
investigation:
ELECTROCARDIOGRAM:
• Increase of amplitude and duration of Р wave in I, II standard
leads and left chest leads (V5,6), the big area of a final negative
part of Р wave in V1 – its signs of hypertrophy left atrium,
infringement intraatrium conduction.
• The right type of the electrocardiogram, caused by hypertrophy RV
is formed.
• Presence in V1 of high R wave, characteristic for hypertrophy RV,
testifies by several pulmonary hypertensia
• It is possible atrial fibrillation: usually fibrillation waves (f) large,
however at diffuse defeat of atriums of a f-wave can be small.
Phonocardiography: increase in amplitude of I tone at a heart apex, II
tones over a pulmonary artery, presence III additional «tone of
opening of the mitral valve» and diastolic murmur on an apex.
76

ECHO CG:
• Allows to measure precisely narrowed left anАV aperture
• Movement of shutters of the mitral valve changes (it gets P-
shaped configuration) - unidirectional movement of shutters of the
mitral valve, expansion of cavities of the left atrium (that is
important for an expediency estimation cardioversion).
X-ray: increase in the left atrium and LV - straightening left contour of
heart because of dilatation of an ear of the left atrium (<< the
mitral configuration »), increase of arches of a pulmonary artery, a
vein of the superior areas of lungs are quite often expanded as a
result of bloodflow redistribution.
Heart cathetherization - the raised pressure of jamming (pressure in
the left atrium) and degree of a pulmonary hypertension, and
quantitatively to estimate degree of the mitral stenosis and
regurgitation.
• Insufficiency аортального the valve.
• (Аортальная insufficiency; аортальная регургитация)
• Ретроградный a blood-groove from an aorta in left желудочек
through leaky closed shutters аортального the valve.
77

Mitral regurgitation
• Mitral regurgitation is backflow of blood from left ventricule to the
left atrium through insolvent (not closed completely) the mitral
valve.
Causes:
• Prolapse of the mitral valve (PMV), rheumatic defeat of heart,
rupture of tendineae chords, dysfunction of papillar muscles, is
more rare - mycsoma of the left atrium and expressed calcification
of the mitral orifice (mainly at elderly women).
• At children the most frequent causes of mitral regurgitation-
dysfunction of papillar muscles owing to abnormal of the left
coronary artery from a pulmonary trunk, acute myocarditis, the
micsomatous valve degeneration.
• The mitral regurgitation caused by dysfunction of papillar muscles is
complication of myocardial infarction with aneurysm of LV (or
without it) and fibrosis of papillar muscles (or without it).
78

Clinical features
Complaints: long enough defect signs can be absent. At the severe
mitral regurgitation often there are attacks of palpitation to the first
symptoms of insufficiency of blood circulation, is possible thanks to
frequent extrasystole and to hyperdynamic effect increased LV.
Complaints further prevail connected with development and
progressing of cardiac insufficiency:
• Dyspnea (appears even before development of symptoms of the
lowered cardiac output and it is caused by a high pressure in the
left atrium,due to the big wave regurgitaton) at first at physical
activity, then in rest;
• Palpitation;
• The complaints caused by stagnation in small and big circles of
blood circulation (cough, hemoptysis, weight in right side due to
hepatomegaly, hypostases of feet).
79

Survey:
• Аcrocyonosis (lips, a tip of a nose, lobes of ears, tips of fingers,
nails).
Palpation: Frequent pulse some the increased filling. The apex beat
carries poured the raising character (is increases) and displaced to
the left.
• The apex beat in left parasternal areas due to increased left atrium
Percussion:The upper border of relative dullness of heart is displaced
upwards, the left border - outside from left midclavicular line.
Auscultation:
• Easing of I tone on apex, splitting and accent II tone over a
pulmonary artery (due to a pulmonary hypertension), systolic
murmar on an apex of heart (at small insufficiency - high and
blowing character, with increase of degree of regurgitation, in
murmur low frequencies, louder prevail, rough). Absence of an
interval between I tone and systolic murmur is typicaly.
80

investigations
Chest X-ray: - with moderated and severe mitral regurgitation are visible the
increased left atrium and LV, mitral configuration of heart.
Electrocardiogram - signs of an overload of the left atrium and left ventricule.
The left type of an electrocardiogram (RI> RII> RIII SIII> and SI) with signs
of hypertrophy LV is registered. At expressed atriomegaly (HLA)it is almost
always registered atrial fibrillation.
ЭХОКГ - increase of cavities of the left atrium and LV, a thickening
(consolidation) of shutters of the mitral valve, absence closing in a phase
of systole of the ventricules. Doppler-EHOKG, especially colour, allows to
estimate of mitral regurgitation is quantitatively. Many of the causes of
the mitral regurgitation (for example, PMV, mycsoma of the left atrium,
rupture of chords and calcification of valvular orifice) have the ECHOCG
signs.
Ventriculography - allows to estimate degree of regurgitation, and pressure in
RV - degree of a pulmonary hypertension which invariably accompanies a
high pressure in the left atrium. The greatest pressure in the left atrium
develops at rupture of chords.
81

82
• There is acute volume overload on left ventricle with an
increase in end diastolic volume. At the same time, there is
new pathway for LV ejection into a low pressure system into
the LA. The left ventricle initially is hypercontractile because
it can eject blood back into the LA and out the aortic valve.
Forward stroke volume is actually decreased.
• In acute MR, the LA cannot accommodate the increased
volume and builds up in the lungs leading to respiratory
distress.

83
• In chronic MR, the LA will slowly dilate, the LV will constantly
be volume overloaded and eventually weaken. Both of these
will eventually lead to congestive heart failure.

87
Physical Exam Review
• A spike and dome arterial pulse
• PMI will be sustained with a triple apical beat secondary a
palpable a wave
• There is a harsh mid systolic murmur radiating throughout the
precordium.
• There is usually also a holosystolic murmur c/w MR
• Maneuvers have specific affects on this murmur

Tricuspid stenosis
ETIOLOGY:
• Rheumatic heart disease (most common). It is
frequently associated with mitral or aortic valve
disease. More common in women.
PATHOPHYSIOLOGY:
• Tricuspid valve stenosis results in a reduced
cardiac output which is restored towards normal
when the right atrial pressure increases. The
resulting systemic venous congestion produces
hepatomegaly, ascites and dependent edema.
88

CLINICAL FEATURES
Symptoms:
• Symptoms of associated left-sided rheumatic valve
lesion.
• Abdominal pain (due to hepatomegaly) and swelling
(due to ascites) and peripheral edema.
On examination:
• JVP: giant "a" wave in JVP.
• Pulsating liver: Deep palpation of liver may show
presystolic pulsation.
• Murmur: Mid-diastolic murmur at tricuspid area i.e.
along lower left sternal border, loud on inspiration.
ECG:
• This shows "P" pulmonale due to right atria!
hypertrophy.
89

TRICUSPID REGURGITATION
ETIOLOGY:
Organic tricuspid regurgitation
• Rheumatic heart disease .
• Infective endocarditis particularly in IV drugs abusers.
• Carcinoid syndrome
• Ebstein's anomaly: Congenially malposition of tricuspid
valve.
Functional (when right ventricle dilates).
• Right ventricular dilatation due to chronic left heart failure.
• “Cor pulmonale”.
• Right ventricular infarction
• Pulmonary hypertension.
90

CLINICAL FEATURES:
Symptoms
• Features of right heart failure. Dyspnea, the feeling of a pulsation in the field of a
neck (which it is caused by high waves regurgitation in the jugular veins, reflecting
of increase pressure in RV), quite often weight and pains in superior part of
abdomen due to hepatomegaly.
Clinical Examination
Survey
• Cyonosis of skin and mucous membranes with an icteric shade, swelling and a
pulsation of cervical veins, positive pulse, a pulsation of a liver and in the area of
right ventricule.
Palpation
• The apex beat is not expressed, the pulsation hypertrophied right ventricule, pulse
small and frequent. Palpation of liver shous systolic pulsation.
Percussion
• Displacement of the right border of relative dullness to the right.
Auscultation
• At the inferior part of breast the weakened I sound, over a pulmonary artery -
easing II sound. At the inferior part of sternum listened systolic murmur
amplifying at a delay of breath at height of a breath (Corvallo’ symptom).
(Murmur: On auscultation, there is a pansystolic murmur along the left parasternal
border. Murmur increases during inspiration (that differentiates from pansystolic
murmur of mitral regurgitation that increases on expiration)).
91

investigations
ESG:The signs of HRA and HRV (tall P wave, increase amplitude of R in V1)
JVP: There is a large v waves. JVP elevated if right ventricular failure has
occurred.Right ventricular heave.
X-ray chest
• Right atrial and ventricular dilatation, dilatation of superior vena cava.
Echocardiography
• Right atrial and ventricular dilatation.
• Abnormal tricuspid valve may be present.
• Estimation of pulmonary artery pressure from Doppler echocardiography.
Cathetherization and angiography: allow to observe the tricuspid
regurgitation, and pressure measurement in RV gives representation
about primary or secondary character tricuspid regurgitation.
•
92

Aortic stenosis
ETIOLOGY
• Rheumatic heart disease is the most, common cause resufting from
adhesions and fusions of the commissures and cusps.
• Congerutally abnormal (bicuspid) aortic valve. Normal valve is
tricuspid, bicuspid valve may be stenotic with commissural fusion at
birth but usually not causing serious narrowing of the aortic orifice
during childhood. The abnormal architecture induces turbulent
flow, which traumatizes the leaflets and leads to fibrosis, increased
rigidity, calcification of leaflets and narrowing of the aortic orifice in
adulthood.
• Senile AS: Age related AS degeneration and calcification of
previously normal valve in elderly, usually smokers, diabetics,
hypertensive and hyperlipidemic.
• SLE and severe familial hyrjerchojesterolemia occasionally cause
aortic stenosis.
93

Other causes of left ventricular outlet obstruction
(other than aortic valve stenosis)
• Subvalvular aortic stenosis: A congenital
condition in which fibrous ridge or diaphragm is
situated immediately below the aortic valve
causing aortic outflow obstruction.
• Supravalvular obstruction: A congenital fibrous
diaphragm above the aortic valve often
associated with mental retardation and
hypercalcemia (Willium's syndrome).
• Hypertrophic obstructive cardiomyopathy:
Asymmetrical septal hypertrophy obstructing the
left ventricular outflow.
94

• Aortic valve stenosis is a heart condition caused by narrowing of the
aortic valve. The aortic valve controls the direction of blood flow from
the left ventricle to the aorta. When in good working order, the aortic
valve does not impede the flow of blood between these two spaces.
Under some circumstances, the aortic valve becomes narrower than
normal, impeding the flow of blood. This is known as aortic valve
stenosis, or aortic
• stenosis, often abbreviated as AS. When the aortic valve becomes
• stenotic, it causes a pressure gradient between the left ventricle (LV) and
the
• aorta. The more stenotic the valve, the higher the gradient between the
LV and the aorta. For instance, with a mild AS, the gradient may be 20
mmHg. This means that, at peak systole, while the LV may generate a
pressure of 140 mmHg, the pressure that is transmitted to the aorta will
only be 120 mmHg. So, while a blood pressure cuff may measure a
normal systolic blood pressure, the actual pressure generated by the LV
would be considered high.
103

Congenital aortic stenosis occurs due to improper development of the aortic valve
in the first 8 weeks of fetal growth. It can be caused by a number of factors,
though, most of the time, this heart defect occurs sporadically (by chance), with no
apparent reason for its development. Some congenital heart defects may have a
genetic link, either occurring due to a defect in a gene, a chromosome
abnormality, or environmental exposure causing heart problems to occur more
often in certain
families. Acquired aortic stenosis may occur after a strep infection that progresses
to rheumatic fever.
Age related calcification of the valve is the most common cause. Deposits of
calcium build up in the valve in some older people. It is not clear why this
happens. This 'calcification' can make the valve stiff and open less easily. It can be
mild and cause little narrowing. But, in time it can become more severe. With
aging, protein collagen of the valve leaflets is destroyed, and calcium is deposited
on the leaflets. Once valve leaflet mobility is reduced by calcification, turbulence
across the valve increases, causing scarring, thickening, and stenosis of the valve.
Why this aging process progresses to cause significant aortic stenosis in some
patients but not in others is not known.
104

Aortic stenosis is the inability of the aortic valve
to open completely. Aortic stenosis is a heart
defect that may be congenital (present at birth)
or acquired (develop later in life). With aortic
stenosis, problems with the aortic valve make it
harder for the leaflets to open and permit
blood to flow forward from the left ventricle to
the aorta.
Aortic stenosis may be present in varying
degrees, classified according to how much
obstruction to blood flow is present. A child
with severe aortic stenosis will be quite ill, with
major symptoms noted early in life. A child with
mild aortic stenosis may have few symptoms, or
perhaps none until later in adulthood. The
degree of obstruction can become worse with
time. Congenital aortic stenosis occurs in 3 to 6
percent of all children with congenital heart
disease. Relatively few children are
symptomatic in infancy, but the incidence of
problems increases sharply in adulthood.
Congenital aortic stenosis occurs four times
more often in boys than in girls.
105

Most children with aortic valve stenosis have no symptoms,
so it’s difficult to detect. In general, many patients will be
easily fatigued, but show no other symptoms until their
thirties to fifties. A small number of children may be prone to
dizziness and fainting (syncope) within the first ten years of
life. If the obstruction is great, infants may suffer from severe
heart failure. Sudden death is uncommon, but possible.
Adolescents with hypertrophic cardiomyopathy, a type of
aortic stenosis where the left ventricle is noticeably enlarged,
have the greatest risk of sudden heart failure.
106

Aortic stenosis is the inability of the aortic valve
to open completely. Aortic stenosis is a heart
defect that may be congenital (present at birth)
or acquired (develop later in life). With aortic
stenosis, problems with the aortic valve make it
harder for the leaflets to open and permit
blood to flow forward from the left ventricle to
the aorta.
Aortic stenosis may be present in varying
degrees, classified according to how much
obstruction to blood flow is present. A child
with severe aortic stenosis will be quite ill, with
major symptoms noted early in life. A child with
mild aortic stenosis may have few symptoms, or
perhaps none until later in adulthood. The
degree of obstruction can become worse with
time. Congenital aortic stenosis occurs in 3 to 6
percent of all children with congenital heart
disease. Relatively few children are
symptomatic in infancy, but the incidence of
problems increases sharply in adulthood.
Congenital aortic stenosis occurs four times
more often in boys than in girls.
107

Serial chest
radiographs of a
patient with
aortic stenosis
taken 10 years
apart. The left
ventricle and
aorta are
prominent in both
radiographs. The
heart is larger and
the right hilar
vessels more
prominent in the
film at the
bottom, which
was taken after
the development
of symptoms.
111

Chest radiograph
showing
generalized
cardiac
enlargement
112

On the lateral view, the
enlarged left atrium
indents the
esophagus
113

Mitral
regurgitation.
On chest
radiograph, the
left atrium is
enlarged–seen
here as an extra
density behind
the heart. In
addition, there
is enlargement
of the main
pulmonary
artery. This
produces an
additional
projection
above the left
ventricular
contour.
114

This lateral film
demonstrates a
prosthetic mitral
valve, which in this
patient is insufficient.
The left atrium is
enlarged, pressing
against the left main
stem bronchus. In
addition, the
retrosternal space is
filled in, typical of
enlargement of the
pulmonary artery and
right ventricle.
115

Chest radiograph
of a 60-year-
old woman
with cardiac
enlargement
resulting from
mitral stenosis
with
pulmonary
hypertension.
116

Syncope in the setting of heart failure increases the risk of death. In patients with
syncope, the 3 year mortality rate is 50%, if the aortic valve is not replaced. While it is
unclear why aortic stenosis would cause syncope, the most popular theory is that
severe AS produces a fixed cardiac output. When the patient exercises, their
peripheral vascular resistance will decrease as the blood vesels of the skeletal
muscles dilate to allow the muscles to receive more blood to allow them to do more
work. This decrease in peripheral vascular resistance is normally compensated for by
an increase in the cardiac output. Since patients with severe AS cannot increase their
cardiac output, the blood pressure falls and the patient wil syncopize due to
decreased blood persufion to the brain. A second theory as to why syncope may
occur in AS is that during exercise, the high pressures generated in the hypertrophied
LV causes a vasodepressor response, which causes a secondary peripheral
vasodilatation that will then cause decreased perfusion to the brain.
117

Patients with aortic stenosis may also experience chest pain,
pressure, or discomfort (called angina or angina pectoris),
caused by an insufficient supply of oxygen to the heart. As
the left ventricle thickens and works harder to expel blood
through the stenotic aortic valve, its demand for oxygen
increases. To compound the problem, aortic stenosis reduces
blood flow to the heart itself as well as to the rest of the
body (the coronary arteries and other arteries of the body
originate from the aorta). Thus, while the heart's demand for
oxygen increases, its supply of oxygen-rich blood decreases,
causing angina.
118

Most patients with aortic stenosis develop one or more of these three classic
symptoms: shortness of breath (dyspnea), passing out (syncope), and chest
pain (angina pectoris). Thickening of the walls of the left ventricle causes the
ventricle to become stiff and unable to relax between contractions. When this
happens, the pressure in the left ventricle rises and blood can "back up" into
the lungs, interfering with normal absorption of oxygen from the lungs into
the bloodstream. This may cause shortness of breath, which worsens as the
left ventricle becomes increasingly impaired. The aortic valve may become so
constricted (stenotic) that it can open only slightly, drastically reducing the
amount of blood that flows into the aorta and throughout the body. In some
cases, the flow of oxygen-rich blood to the brain may not be enough to sustain
normal brain function. When this occurs, patients may briefly lose
consciousness, or pass out. Losing consciousness is called syncope.
119

Complaints: a classical triad of symptoms of the aortic stenosis - faints, a
stenocardia and a dyspnea at physical activity. The faints arising at physical
activity, are considered as a sign of the fixed cardiac output and reflect
the severe aortic stenosis. The stenocardia is caused by insufficient
subendocardialby arterial blood supply of hypertriphied walls of LV.
Average life expectancy of patients after stenocardia occurrence - 5 years,
a faint - 4 years, cardiac insufficiency - 3 years.
Survey:
• Pallor of skin, apex beat of the heart it is often displaced to the left and
downwards in 5-6 intercostals space.
Palpation:
• The apex beat is displaced to the left and downwards, larged,
strengthened and resistant. Over an aorta in 2 intercostal space to the
right of a breast it is defined systolic trembling (<<the cat's purring »), is
dicrease of systolic blood pressure and increase diastolic blood pressure,
i.e. low puls pressure; pulse small, slow, rare.
Percussion:
• Displacement of the left border of relative dullness of heart to the left.
Auscultation:
• On an apex I sound is decrease, II sound over an aorta is decrease, over an
aorta rough systolic murmur.
120

investigations
Electrocardiogram: the left type of an electrocardiogram, signs of a
hypertrophy left ventricule, depression of segment ST from an isoline and
inversion of Т wave in I, II standard leads and the left chest leads. In severe
cases - LBBB. These changes testify to considerable overload LV and
chronic coronary insufficiency.
Phocardiography: over an aorta – hight amplitude systolic murmur, beginning
after 0,04 0,06 sec. after I tone and coming to an end for 0,05-0,06 sec. to
II tone, amplitude of II tones it is dicrease.
ECHO CG: sharp decrease of degree of disclosing аоrtic cusps during a
systole, consolidation of aortic cusps of the valve does reflexion from
them by more intensive, signs of HLV. Doppler-EHOKG allows to define
pressure gradients precisely.
Chest X- ray: increase of size of the LV, the heart form has of aortic
configuration, contraction of left ventricule are increased.
Catheterization: allows to measure of pressure gradients, and also to reveal
damage of coronary arteries.
121

Aortic regurgitation
The retrograde bloodflow from an aorta to the left ventricule
through dontcomplate closed of cusps of the aortic valve.
Causes: rheumatic damage of the aortic valve, infectious
endocarditis,
Mycsomatous degeneration and a trauma. At children –
defect of interventricular septal with prolapse of the aortic
valve. Severe or prevailing аortic regurgitation can be
accompanied it calcification. The most widespread causes
of easy forms аоrtic regurgitation at adults - the congenital
bycuspid valve, a severe arterial hypertensia with diastolic
blood pressure more than 110 mm HG. Rare аortic
regurgitation find at patients with diffuse diseases of a
connecting tissues. Last years the causes concern syphilitic
аоrtitis, stratifying an aorta aneurysm etc.
122

• The size and strock volume of LV at aortic
regurgitation are increased, as during time of
diastole in it blood from pulmonary veins and
blood regurgitad from an aorta also.
Hypertrophy LV always develops
proportionally it dilatation - for maintanance
pressure. Сог bovinum - «the bull heart»,
characteristic for aortic regurgitation, -
represents the biggest on the size and weight
heart, known in a cardiac pathology.
123

• Complaints: long years high tolerance to
physical activity can remain; eventually,
appear a dyspnea at physical activity,
orthopnea and night attacks of a cardiac
asthma. Complaints to palpitation, dizziness,
pains in the aries of heart (at 5 % stenocarditic
character) are possible at massive
regurgitation. Attacks of a stenocardia arise at
night (probably because at night at decrease
of heart rate increases of regurgitation) is
more often.
124

Survey:
• Pallor of a skin and mucous membranes, «dancing of carotids» ( the
sinocarotidic reflexlow diastolic pressure is caused peripheral
dilatation of vessels and backflow of blood to the cavity LV),
capillary pulse or Qwinke’s symptom (pulsing palloring and
reddening of a nail bed of a finger of a hand at easy pressing on a
nail tip), visible on a neck a sharp pulsation carotid arteries is called
corrigan’s pulse, head rocking in a step to cardiac contraction,
caused by ballistic action of the big strock volume of blood, is called
the Musset's symptom. An apex beat increased, displaced
downwards and to the left, at survey of area of a stomach - a liver
pulsation.
Palpation:
• The apex beat is increased, displaced downwards and to the left,
larged, rising; the pulses waves with fast lifting and the big
amplitude (<<clapping»pulse), prompt lifting and fast falling of
arterial pulse - high, fast, skipping, jumping pulse.
Percussion:
• Displacement of the left border of relative dullness to the left.
125

Auscultation:
• On apex I tone is weakened, II tone over an aorta is weakened, at
massive aortic regurgitation- disappears; diastolic murmur over an
aorta and in Botkin-Erba point, is spent to axillary area; on apex -
diastolic Flint’s murmur (the descending stream regurgitating from
a blood aorta raises a forward cusp of the mitral valve, not allowing
it completely to reveal, I.e. it is formed relative mitral stenosis).
Flint’s murmur disappears at pressure decrease in an aorta or
reduction aortic regurgitation whereas murmur true mitral stenosis
becomes louder. At auscultation of large vessels Traube’s double
sound (the sharp sound heard over a femoral artery, a sound of a
pistol shot) and double Vinogradova-Djuroze’s sounds (systolic
murmur over a femoral artery distal from pressing places on it a
finger together with diastolic murmur to procsimal this place) is
listened.
• Systolic blood pressure is increase owing to increase of strock
volume, diastolic blood pressure is lowered, high pulse pressure.
126

investigations
Electrocardiogram: the left type of an electrocardiogram (RI> RII> RIII
is marked; SIII> SI; RV56> RV4), and also interval displacement SТ
downwards and negative Т wave; LBBB is possible.
Phonocardiography: on apex - decrease amplitude of 1 tone, over an
aorta is registered high-frequency the diastolic murmur, which
amplitude decreases by the end of diastole, decrease amplitude of
II tone.
ECHO CG: consolidation and fybrosis of cusps of the aortic valve of a
rheumatic aetiology, trembling of a forward cusp of the mitral valve
during time of diastole of ventricules due to of stream blow at
regurgitation of blood from an aorta to the LV.
Chest X-ray: sharp increase in the sizes of LV - «the aortic
configuration», a heart waist expansion and the dilated and
increase pulsation of an aorta.
127

Differential diagnosis of valvular heart disease.
Mitral Stenosis Mitral Regurgitation
Inspectio
n
Malar flush, precordial
bulge, and diffuse pulsation
in young patients.
Usually prominent and
hyperdynamic apical impulse
to left of MCL.
Palpation
"Tapping" sensation over
area of expected PMI. Right
ventricular pulsation left
third to fifth ICS
parasternally when
pulmonary hypertension is
present. P2 may be
palpable.
Forceful, brisk PMI; systolic
thrill over PMI. Pulse normal,
small, or slightly collapsing
128

Heart sounds,
rhythm, and
blood
pressure
S1 loud if valve
mobile. Opening snap
following S2. The
worse the disease,
the closer the S2-
opening snap interval.
S1 normal or buried in early part
of murmur (exception is mitral
prolapse where murmur may be
late). Prominent third heart
sound when severe MR. Atrial
fibrillation common. Blood
pressure normal. Midsystolic
clicks may be present and may
be multiple.
129

Murmurs
Location
and
transmiss
ion
Localized at or near apex.
Diastolic rumble best
heard in left lateral
position; may be
accentuated by having
patient do sit-ups. Rarely,
short diastolic murmur
along lower left sternal
border (Graham Steell) in
severe pulmonary
hypertension.
Loudest over PMI; posteriorly
directed jets (ie, anterior mitral
prolapse) transmitted to left
axilla, left infrascapular area;
anteriorly directed jets (ie,
posterior mitral prolapse) heard
over anterior precordium.
Murmur unchanged after
premature beat
130

Timing Relation of opening snap to A2
important. The higher the LA
pressure the earlier the opening
snap. Presystolic accentuation
before S1 if in sinus rhythm.
Graham Steell begins with P2
(early diastole) if associated
pulmonary hypertension.
Pansystolic:
begins with S1 and
ends at or after
A2. May be late
systolic in mitral
valve prolapse.
Charact
er
Low-pitched, rumbling;
presystolic murmur merges with
loud S1.
Blowing, high-
pitched;
occasionally harsh
or musical. 131

Differential diagnosis of valvular heart disease
Optimum
auscultatory
conditions
After exercise, left lateral
recumbency. Bell chest piece
lightly applied.
After exercise; use
diaphragm chest piece.
In prolapse, findings may
be more evident while
standing.
Radiography Straight left heart border from
enlarged LA appendage. Elevation
of left mainstem bronchus. Large
right ventricle and pulmonary
artery if pulmonary hypertension
is present. Calcification in mitral
valve in rheumatic mitral stenosis
or in annulus in calcific mitral
stenosis.
Enlarged left ventricle
and LA.
132

Mitral Stenosis Mitral
Regurgitation
ECG Broad P waves in standard leads;
broad negative phase of diphasic
P in V1. If pulmonary hypertension
is present, tall peaked P waves,
right axis deviation, or right
ventricular hypertrophy appears.
Left axis deviation
or frank left
ventricular
hypertrophy. P
waves broad, tall, or
notched in standard
leads. Broad
negative phase of
diphasic P in V1.
133

Two-
dimensional
echocardiog
raphy
Thickened, immobile mitral valve
with anterior and posterior leaflets
moving together. "Hockey stick"
shape to opened anterior leaflet in
rheumatic mitral stenosis. Annular
calcium with thin leaflets in calcific
mitral stenosis. LA enlargement,
normal to small left ventricle.
Orifice can be traced to
approximate mitral valve orifice
area.
Thickened mitral valve in
rheumatic disease;
mitral valve prolapse;
flail leaflet or
vegetations may be
seen. Dilated left
ventricle in volume
overload. Operate for
left ventricular end-
systolic dimension > 4.5
cm.
134

Continuous
and color
flow
Doppler
and TEE
Prolonged pressure half-time
across mitral valve allows
estimation of gradient. MVA
estimated from pressure
half-time. Indirect evidence
of pulmonary hypertension
by noting elevated right
ventricular systolic pressure
measured from the tricuspid
regurgitation jet.
Regurgitant flow
mapped into LA.
Use of PISA helps
assess MR severity.
TEE important in
prosthetic mitral
valve regurgitation.
135

Lecture no.4.cvs,h spptx CVS

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (20)

Similar to Lecture no.4.cvs,h spptx CVS

Similar to Lecture no.4.cvs,h spptx CVS (20)

More from bharat kumar

More from bharat kumar (6)

Recently uploaded

Recently uploaded (20)

Lecture no.4.cvs,h spptx CVS