about pericarditis

1. LECTURE №3. The syndrome of inflammatory changes an
endocardium, myocardium and pericardium.
Myocarditis. Pericarditis. Rheumatic
fever.
Cardiomyopathy.

2. The information block
Inflammatory process can develop in the endocardium, a
myocardium and a pericardium. Most often the cardiac
muscle is involved in inflammatory process.
Syndrome of an inflammation of a cardiac muscle
(myocarditis) – this is clinico-laboratory-instrumental
complex caused by inflammatory process in a
myocardium.
• The causes:
- Infectious (virus almost in 70 %, bacterial, rickettsiosis,
fungoid, scarlet fever parasitic, etc.);
- Not infectious and allergic, caused by influence physical
and chemical factors (toxic, radiating).

3. CLINICAL PICTURE
• Complaints
• pains in the field of heart, boring or pricking character, often
constant;
• pains can arise without relation to the physical activity and do
not vary on intensity at physical or emotional loadings,
nitroglycerine taking;
• pains without accurate irradiation, irregulatory in heart work,
• breathlessness at first at more physical activity;
• at illness progressing – at the minimal physical activity, then in
rest,
• at night there is cough in horizontal position,
• a palpitation, attacks of an asthma,
• a pain and weight in right side of abdomen, oedema of the feet,
• increase in stomach volume (аscites),
• fast fatigue, the general weakness, especially at physical activity.

4. CLINICAL PICTURE
• The above described complaints can
be accompanied by a so-called
syndrome of an inflammation and an
intoxication: increase of temperature,
absence of appetite, sweating,
weakness.

5. Survey.
• Pallor of skin, sometimes light acrocyonosis,
swelling and a pulsation of cervical veins,
oedema of feet.
Palpation: apex beat
• Decreased, displaced to the left,
• Pulse
soft, frequent.
Percussion:
• Expansion of the heart relative dullness borders
, mainly to the left.

6. Survey.
Auscultation:
• Soft S1 on the heart apex,
• accentuated S2 over a pulmonary artery,
• «a gallop rhythm»,
• a tachycardia,
• systolic murmur on an apex or in the field of
III-IV intercostals space at the left at a
breast.
• The blood pressure it is lowered, especially
systolic, it is reduced pulse pressure.

7. Laboratory and instrumental
Inspection methods of investigation:
• Common blood count:
• increase of leucocytes, increase of ESR, hyperglobulinemia
(alpha and gamma-globulinemia), increase of levels of cardiac
enzymes (creatine phosphatekinase, lactate dehydrogenase,
asparate aminotransferase, troponins).
• Electrocardiogram: the sinus tachycardia, extrasistoly, heart
block, atrial fibrillation.
• Pfonocardiography: S1 - reduction of the amplitude,
registration of "a gallop rhythm», systolic murmure on apex
of the heart.
• Echocardiography: decreased cardiac output.
• Roentgenological research: increase in the sizes of heart
(cardiomegaly).

8. MYOCARDITIS CRITERIA
MAJOR CRITERIA:
PATHOLOGICAL EKG changes ( Rhythm and
conductions diisturbencies)
Sarcoplasmatic enzymes and isoenzymes
activity increasing (LDH, CPK)
CONGESTIVE HEART FAILURE or CARDIOGENIC
SHOCK.

9. MYOCARDITIS CRITERIA
MINOR:
TACHICARDIA
SOFT S1
Gallop Rhythm
ADDITIONAL CRYTERIA
• ECHO –local myocardial asynergy
• Scan with Gallyi-67
• Myocardium biopsy
Two major or one plus two minor plus
preceeding infection evidence for diagnosis
nesessary

10. Rheumatic fever
• Is an inflammatory, possibly
autoimmune disease, in nature,
involves many tissues, including the
heart, joints, skin, and central
nervous system.
• Preceding infection of the upper
respiratory tract with group A
Streptococcus is a prerequisite to the
development of acute rheumatic
fever.

11. Signs and symptoms
• Joint symptoms ranging from arthralgias to frank
arthritis (75%)
• Joints involved are medium to large, e.g., ankles,
knees, wrists
• Joint involvement is classically migratory
• Joint symptoms usually disappear in 1 – 4 weeks
without permanent deformities
• Carditis (65%), mild or severe with murmurs
• Cardiac involvement may include pericarditis,
myocarditis, and/or valvular insufficiency.
Appears within 2 weeks and lasts 6 weeks to 6
months

12. Mitral valve in the acute phase of
Rheumatic fever

13. Signs and symptoms
• Valvular damage may be permanent.
• P – R prolongation on ECG
• Erythema marginatum (classic rash) <5%
• Subcutaneus nodules (painless, hard swellings
overlying bony prominences) 5 – 10%
• Chorea is often a late finding but may be a
presenting complaint. It occurs in 10 – 15% of
patients, and its duration is not altered by treatment.
• Fever 101 – 104 0F (38.3 – 40.0 0C)
• Abdominal pain is common. It may be severe.

14. Signs and symptoms
• Epistaxis (historycally important, but rarely
seen in acute rheumatic fever)
• Facial tics
• Facial grimace

15. Pericarditis
• The commonest causes are viral or bacterial infection,
Ml, or uraemia.
• Pain, not related to movement or exertion
• Friction rub of a pericardium,
• electrocardiogram-change,
• effusion in a pericardium with development
tamponade of heart
• and paradoxical pulse - the basic signs of an
inflammation of a pericardium.
• The pain represents the major symptom. Usually it is
marked at the acute infectious process, connected with
hypersensitivity or autoimmunity processes, however
often is absent at slowly developing tuberculosis,
postradiating and uraemic pericarditis.

16. • The pain-сonstant soreness, compressing,
• as a rule, is localised retrosternal ,
• irradiation to one, or in both hands and reminds
these an ischemic pain.
• Often has character pleural, increase, worse at a
breath (inspiration -pleuritic) and is acute,
• It is accompanied by cough, varies at change of
position of a body.
• It is characteristic, that the pain relieved slightly
by sitting forwards.
Pericarditis

17. Pericarditis
• Pericardial friction rub - important physycal sign,
sometimes it comes to light only at strong pressure of a
diaphragm with stethoscope on a chest wall.
• This is a scratching sound, comparable with creaking
leather, heard with each heartbeat caused by inflamed
pericardial membranes rubbing against each other.
• Pericardial friction rub is heard best in exhalation,
louder as the patient is sitting up, leaning forward, or in
lying position on the left side.
• Pericardial friction rub usually has changeable, passing
character. The loud creaking sound can disappear within
several hours and appear then next day.

18. Clinical features:
• These are mainly of right heart failure with JVP
(with prominent x and y descents,);
• Kussmaul's sign (JVP rising paradoxically with
inspiration);
• soft, diffuse apex beat;
• quiet heart sounds; muffled S1 & S2.
• S3;
• diastolic pericardial knock,
• hepatosplenomegaly,
• ascites,
• and oedema.

19. • Electrocardiogram - at acute process without massive effusion
usually is revealing concave (saddle-shaped) ST segment
elevation , in 2,3 standard leads and from V2 to V6, with
depression SТ in aVR and V1, without QRS complexes
change,
• is rare against the lowered voltage of ECG, but may be
normal or non-specific (10%).
• Fluid in a pericardium cavity - heart sounds become
decreased.
• The pericardial friction rub can disappear or is clear be
listened.
• Apex beat can disappear, but sometimes is palpatedmedially
from the left border of cardiac dullness.
• On the the chest X ray film (CXR) shows an enlarged, globular
heart (if >250mL fluid), decreased ventricular pulsations.
Pericarditis

20. Pericarditis
• EchoCG -echo-free space (>2cm, or >1cm if acute),
between a posterior part of pericardium and
posterior part epicardium left ventricule means
fluid presence in a pericardial cavity
(inflammatory effusion).
• diastolic collapse of right atrium and right
ventricle
• Paradoxical pulse is more expressed, than in norm
(10 mm hg) reduction the systolic blood pressure
at a breath. At a breath at palpation reveal easing
or disappearance of arterial pulse during a breath.

21. Management:
• Seek expert help. The pericardial effusion
needs urgent drainage .
• Send fluid for culture, ZN stain/TB culture &
cytology.

22. EKG

23. Infective endocarditis
• The infectious inflammation of the endocardium - (a
septic condition), a bacterial inflammation of the
endocardium.
• Etiology:
– Is due to microbial infection of a heart valve, the lining of
a cardiac chamber or blood vessel, or a congenital
anomaly ( septal defect).
– The causative organism is usually a bacterium
streptococci, staphylococci, gram-negative bacilli,
heamophilus, anaerobes), may be a rickettsia, chlamydia
or fungus.

24. Classification
• 50% of all endocarditis occurs on normal valves. It
follows an acute course, and presents with acute
heart failure.
• Endocarditis on abnormal valves tends to run a
subacute course. Predisposing cardiac lesions:
aortic or mitral valve disease; tricuspid valves in IV
drug users; coarctation; patent ductus arteriosus;
VSD; prosthetic valves. Endocarditis on prosthetic
valves may be early (acquired at the time of surgery,
poor prognosis) or late (acquired haematogenously

25. Causes
• Bacteria:
• Any cause of bacteraemia exposes valves to the risk of
bacterial colonization (eg dental work; UTI; urinary
catheterization; cystoscopy; respiratory infection; endoscopy
(controversial); colonic carcinoma; gall bladder disease; skin
disease; IV cannulation; surgery; abortion; fractures).
• Quite often, no cause is found.
• Streptococcus viridans is the commonest (35-50%). Others:
enterococci; Staphylococcus aureus/epidermidis;
diphtheroids and microaerophilic streptococci.
• Rarely: HACEK group of Gram -ve bacteria
(Haemophilus“Actinobacillus Cardiobacterium
EikenellaKingella); Coxiella burnetii; Chlamydia.
• Fungi: These include Candida, Aspergillus, and Histoplasma.
Other causes: SLE (Libman-Sacks endocarditis); malignancy.

26. Clinical features
• The patient may present with any of the following:
• Signs of infection: Fever, rigors, night sweats, malaise,
weight loss, anaemia, splenomegaly, and clubbing.
• Cardiac lesions: Any new murmur, or a change in the
nature of a
• Vegetations may cause valve destruction, and severe
regurgitation, or valve obstruction. An aortic root
abscess causes prolongation of the PR interval, and may
lead to complete AV block.
• LVF is a common cause of death.
• Immune complex deposition: Vasculitis may affect any
vessel.
• Microscopic haematuria is common;

27. Clinical features
• Glomerulonephritis and acute renal failure may
occur.
• Roth spots (boat-shaped retinal haemorrhage with
pale centre);
• splinter haemorrhages (on finger or toe nails);
• Osler's nodes (painful pulp infarcts in fingers or
toes) and Janeway lesions (painless palmar or
plantar macules) are pathognomonic.
• Embolic phenomena: Emboli may cause abscesses
in the relevant organ, eg brain, heart, kidney,
spleen, GI tract. In right-sided endocarditis,
pulmonary abscesses may occur.

28. Duke criteria for infective endocarditis
• Major criteria:
• Positive blood culture:
– typical organism in 2 separate cultures or
– persistently +ve blood cultures, eg 3, >12h apart (or
majority if 4)
• Endocardium involved:
– positive echocardiogram (vegetation, abscess,
dehiscence of prosthetic valve) or
– new valvular regurgitation (change in murmur not
sufficient).

29. Duke criteria for infective endocarditis
• Minor criteria:
• Predisposition (cardiac lesion; IV drug abuse)
• Fever >38В°C
• Vascular/immunological signs
• Positive blood culture that do not meet major criteria
• Positive echocardiogram that does not meet major
criteria.
• How to diagnose:
• Definite infective endocarditis: 2 major or 1 major and
3 minor or all 5 minor criteria (if no major criterion is
met).

30. • Features of haemodynamics play the big role in development of a septic
inflammation of endocardium. Blood-groove infringement in sites,
damaging to other structural changes or anomalies, promotes surface
change of endotelium and to formation of thrombotic imposings, which
then become the centre of sedimentation of microorganisms.
• Microorganisms circulating in blood are attached to endotelium, then
become covered by fibrin imposing, forming vegetations. Microorganisms
fastly cause destruction of valves, them forming as emboli. Therefore
following basic pathological features may be seen:
Local destructive effects of intracardiac infection:
- Destruction of the valve cusp, produssing ulceration and ultimately regurgitation.
- Rupture of chordae tendineae.
- Paravalvular abscess leading to destruction of conduction system ( causing
arrytmias) and purulent pericarditis.
- Large vegetations may causer functional valvular stenosis.

31. • Embolism
-Embolisation fragments of vegetations producing splenic, renal,
myocardial or pulmonary infarctions.
• Metastatic infection
-Septic emboli may cause infection in any organ or tissue producing
abscess there.
• Deposition of immune complexes
-Deposition of immune complexes ( antigen antibody complexes) in
various tissues producing extracardiac manifestations e. g. arthaldia,
Roth spots, Janeway lesions, focal glomerulonephritis, acute
vasculitis.
TYPES:
1. Subacute endocarditis
2. Acute endocarditis
3. Prothetic endocarditis

32. • At circulation in blood of microbes and blood
crops define a kind and number of bacteria.
Occurrence emboli - the important sign, is
more often observed emboli of vessels of a
brain, a spleen,GIT, hearts, finitenesses
kidneys.

33. • Survey - petechiae - displays acute vasculitis, immunopositive by
the nature. Other defeats of a skin accompanied by pains, pressure
, can be a consequence of emboli.
• Complaints: the general weakness and fatigue, reduction of weight
of a body, a fever, sweat at night, appetite loss, arthralgia. The
emboly can cause paralyses, pulmonary infarction, heart (a pain in a
chest), and also a painful syndrome depending on where has got
emboli.
• Physical signs: in early terms can be any signs. At the chronic - there
is a pallor of skin, a fever. Increase of pulse rate. Skin changes -
petechiae- the small size, the red colour, looking like hemorrhages,
not growing white at press, not strained, painless. They are
localised on mucous of throat, oral cavity, conjunctivus, on a skin
of the upper part of a thorax. On mucous a mouth and conjunctiva
in the centre the pale ( Roth’s spots), gradually they get brown
colour and disappearance. Under nails linear hemorrage, as at a
trauma. As consequence emboli on palms, fingers of hands, heels,
other places - erytromatous, painful, intense small nodes (Osler’s).
The emboli in larger arteries can cause a gangrene of fingers of
finitenesses, change of fingers of hands in the form of clubbing, in
rare instances – jaundice.

34. On soft tissues of fingers of hands - erhytromatous not intense
hypodermic maculopapulous defeats ( Jeneway’s lesions), inclined
to ulceration.
• Heart area - considerable changes of character of cardiac noise, for
the first time arisen dyastolic noise - owing to the ulceration valve,
rupture of valvular chords or formation of very big vegetations.
Destruction of heart valves can become complicated rupture
valvular chords or punching of shutters, that quickly leads to
progressing heart failure. At addicts - it is damaged the right atrio-
ventricular valve with signs right side cardiac failure.
• Laboratory investigation.
-CBC: leucocytosis, neutrophylosis, increase ESR. At a chronic course -
an anaemia, and then a syndrome of hyperspleen.
- The positive hemoculture (revealing of the activator and its sensitivity
to antibiotics).
- ECHO: vegetations.

35. • Pathology:
• The acute phase of rheumatic fever is
characterized by exudative and рroliferative
inflammatory reactions involving connective or
collagen tissue. Heart, joints, brain, skin and
subcutaneous tissues are primarily affected.
• In rheumatic carditis,_principally affected part is
heart valve especially the aortic and mitral valves.
The characterjstic lesion of rheumatic carditis, is
the Aschoff nodule, which is a granulomatous
lesion with a central necrotic area. The valve
cusps become tickelied by ederma and_by the
infiltration of capillaries. Later a row of tiny
vegetations is foimed along the lines of closure of
the valve leaflets.

36. Criteria for Rheumatic fever
Diagnostic
categories
Criteria
Major
manifestations
Carditis, polyarthritis, chorea, erythema
marginatum, subcutaneous nodules
Minor
manifestations
clinical: fever, polyarthralgia
laboratory: elevated acute phase reactants
(erythrocyte sedimentation rate or leukocyte
count)
electrocardiogram: prolonged P-R interval
* Supporting
evidence of а
preceding
streptococcal
elevated or rising antistreptolysin-O or other
streptococcal antibody, or а positive throat
culture, or rapid antigen test for gr. А
streptococci, or recent scarlet fever.

37. Complications
• Congestive heart failure
• Rheumatic heart disease
• Arrhythmias
• Pericarditis
• Pericardial effusion
• Rheumatic pneumonitis

38. INVESTIGATIONS
Although the diagnosis of rheumatic fever is clinical,
following investigations may be helpful:
Throat swab culture
• Throat swab culture for group A streptococcus.
Antistreptolysin О titer (ASOT):
• The_rising_ titer of antibodies against streptococci
(ASOT) indicates a recent streptococcal infection. ASOT
is elevated in about 80% of cases. If ASOT is normal, it
should be rechecked after a week, as it may then be
elevated. If not elevated then anti-DNase В is
performed. Both types of titers are elevated for weeks
or months.

39. ESR and C-reactive protein:
• ESR and C-reactive protein are the acute phase
reactants indicating tissue inflammation and are
elevated during the acute stages of the disease.
• Erythrocyte sedimentation rate (ESR) is useful in
monitoring the course of the didease; it usually
returns to normal as the rheumatic activity
subsides. ESR may be elevated in patients with
anemia and may be supressed to normal levels in
patients with_congestive heart failure. Unlike the
ESR, the CRP level is unaffected by anemia or
cardiac failure.

40. Blood CP
• Leukocytosis
• Anemia is usually mild to moderate and is normocytic
normochromic in morphology.
Chest x-ray: may be normal or indicates cardiomegaly,
pulmonary edema and increased pulmonary
vascularity.
ECG: may indicate prolonged PR interval, heart block,
features of pericarditis and myocarditis.
Echocardiography: It may show mitral regurgitation due
to prolapse of anterior mitral leaflet, heart dilatation
and valve abnormality. Myocardial dysfunction and
pericardial effusion may also be seen.

41. ACUTE MYOCARDITIS
Acute myocarditis causes focal or diffuse
inflammation of the myocardium. Majority of
cases are due to infection caused by viral
(most common), bacterial, rickettsial, fungal,
or parasitic agents; but toxins, drugs and
immunologic disorders can also cause
myocarditis.

42. CAUSES OF MYOCARDITIS
Primary myocarditis
• Myocarditis caused by acute viral infection is called primary
myocarditis.
• Viruses: Coaxsackie A and B, adenovirus, influenza virus, HlV virus,
Epstein-Barr_yirus, herpes virus, cytomegalovirus, mumps virus,
respiratory syncytial virus and rubella virus.
Secondary myocarditis
• Myocarditis caused by non-viral cause is called secondary
myocarditis
Infections
• Bacterial: Diphtheria, brucellosis, H.influenza, mycoplasma,
pneumococci, salmonella, streptococcus, staphylococcus.
• Protozoal: Entamoeba, trypanosomiasis .
• Fungal: Candida, actmomyces, aspergillus

43. Endocrine and metabolic disorders
• Diabetes, hypo and hyperthyroidism, acromegaly, carcinoid
syndrome, inherited siorage diseases.
Connective tissue diseases
Scleroderma, SLE, polyarteritis nodosa.
Infiltrative disorders
• Hemochromatosis, hemosiderosis, sarcoidosis, amyloidosis.
Endomyocardial fibrosis and eosinophilic heart disease.
Toxins
Neuromuscular disorders

44. Clinical features
• The clinical presentation of infectious myocarditis is variable.
• Many patients are asymptomatic and will have a complate
resolution of myocarditis without complications.
• Patients may present with heart failure several days to a few
weeks after the onset of an acute febrile illness or a
respiratory infection; or heart failure without antecedent
symptoms.
• Pleural chest pain secondary to pericarditis is common.
• Patient may present with life threatending atthythmias or
embolic events.
• Patients may present after months or years of development of
dilated cardiomyopathy.

45. On examination
• Tachycardia
• Pericardial friction rub may be heard
• Features of congestive cardiac failure
• S3 gallop murmurs of tricuspid and mitral
regurgitation may be present (due top
dilatation od chambers)

46. Investigation
• ECG: Non-specific ST segment and T wave abnormalities,
arrhythmias or conduction delay.
• X-ray: shows normal heart size initially and then cardiomegaly.
• Cardiac enzymes: may be elevated if the patient presents acutely
usually within one month of symptoms.
• Echocardiography: trashtoracic echo is usefulto assess the size of
chambers and their function. In fulminant myocarditis there is
increased ventricular wall thickness due to inflammation
associated with interstitial edema.
• MRI: has sensitivity of 100% while specifity 90-100% in the
diagnosis of acute myocarditis.
• Endomyocardial biopsy: It is the gold standard for diagnosing
muocarditis and is useful when a treatable cause is found.

47. Clinical pathological types of
myocarditis
• Fulminant myocarditis
• Subacute myocarditis
• Chronic active myocarditis
• Chronic persistent myocarditis

48. Cardiomyopathy
• The cardiomyopathy is a general term indicating disease
of the cardiac muscle primarity, not associated with the
major causes of cardiac disease such as ischemic heart
disease, hypertension, pericardial disease, valvular
disease, or congenital defects. While some have specific
causes, many cases are idiopathic.
• TYPES:
• Dilated cardiomuopathy (ventricular dilatation)
• Hypertrophic cardiomyopathy (myocardial hypertrophy)
• Restrictive cardiomyopathy (impaired ventricular filling)

49. Dilated cardiomyopathy
• Is characterized by dilatation and impaired ventricular contraction (left
ventricular dysfunction) leading to progressive left-sided and later, right-
sided failure. Functional mitral and/or tricuspid regurgitation may occur.
Arrhythmias are common. Cause cannot be identified in most of the
patients; myocarditis and chronic alcohol abuse are probably freqent
causes of dilated cardimyopethy.
• Possible causes of dilaed cardiomyopathy:
• Idiopathic ( most common)
• Alcohol
• Viral myocarditis
• Familial and genetic factors
• Peripartium cardiomyopathy
• Diabetes mellitus
• Sarcoidosis, hemochromatosis
• Connective tissue disease (multiple sclerosis)

50. Clinical features:
• Features of cardiac failure, arrhythmias or emboly
• Cardiac failure, S3 gallop rhythm
• Ventricular dilatation leads to functional mitral or tricuspid valvular
regurgitation
Investigations:
X-ray chest: shows large flask-shaped heart (massive cardimegaly)
Echocardigraphy: reveals dilatation of left ventricle, dilatation of right
ventricle with poor global contraction. It helps in assessment of degree of
left ventricular function, and axclusion of concominant valvular or
pericardial disease.
ECG: tachycardia, conduction abnormalities, ST- segment and T wave
changes, ventricular ectopics.
Cardiac biopsy: fibrosis and non- specific leukocyte infiltration.
Cardiac catheterization: left ventricular dilatation and dysfunction, high end-
diastolic pressure, low cardiac output.

51. Hypertrophic cardiomyopathy
• Is characterized by marked hypertrophy of the left and/or right ventricle
particularly the interventricular septum in the absence of a cardiac or
systemic cause (asymmetrical septal hypertrophy).
• The hypertrophied septum and the anterior movement of mitral valve
across the outflow tract making with the ventricular septum midsystole
result in mechanical obstruction to left ventricular ejection. Some degree
of mitral regurgitation may develop.The left ventricular outflow tract is
narrowed during systole between the bulging septum and systole anterior
motiob (SAM) of the anterior mitral leaflet causing obstruction to left
ventricular emptying therefore called obstructive cardiomyopathy. The
obstruction is worsened by factors that increase myocardial contractility or
that decrease left ventricular filling.

52. • Inabout 50% cases it is an onherited as autosomal dominant trait, soma
patients have prolonged history of hypertension and soma cases are
sporadics. It is_the most common genetically transmitted cardiac
disorder. Incidence is I in 500 of the gcnerl population.
• This type of hypertrophy usually manifests in adolescents and young
adults, most of the patients are identified during screening of relatives of
patients with hypertrophic cardiomyopathy. It may manifest 4thor 5th
decade and sometimes in elderly.
• The physiological characteristic of HOCM is diaslolic dysfunction (while
systolic dysfunction in dilated cardiomyopathy) resulting in abnormal
sliffness of left ventricle with resultantl impaired ventricular filling. Left
ventricular end-diastolic pressure increases resulting in pulmonary
congestion and dyspnea.

53. CLINICAL FEATURES
• Symptoms:
• Patient may be asymptomatic, diagnosed on echo during screening.
• Dyspnea: it is due to pulmonary congestion resulting from elevations in
pulmonaru venous and left atrial pressure because of stiffness of
hepertrophic ventricles (diastolic dysfunction).
• Chest pain: This occurs on exertion or at rest due to compression of
intramyocardial coronary arteries and increased oxygen requirement due
to increased myocardial contraction and muscle mass. Chest pain usually
does not respond to sublingual nitroglycerine.
• Syncope: Especially post-exertional due to inadequate cardiac output with
exertion or from cardiac arrhythmia.
• Palpitation: It is_due to arrhythmias. Atrial fibrillation js_common and
poor prognostic sign. Ventricular arrhythmias are also common and
sudden death may occur.
• Sudden death: This can occur at any age but the highest rates occur in
adolescents and young adults. ~ "
• Congestive heart failure •-

54. On CVS Examination
Palpation:
• Apex beat is displaced laterally, forceful and diffuse. A double apical
pulsation (forceful atrial contraction produces a palpable fourth heart
sound).
Auscultation:
• S1 is normal, often preceded by S4, normal S2.
• Late systolic murmur beast heard between the apex and left sternal
border radiating to lower sternal border, ахillа and base of heart
but not into the neck vessel (that differentiates it from murmur of aortic
stenosis). It is produced due to left ventricular outflow obstruction in late
systole. This murmur is increased by Valsalva maneuver and by standing
while decreased by squatting.
• A pansystolic murmur at apex may be heard due to mitral regurgitation as
a result of systolic anterior motion of anterior leaflet of mitral valve).
• Reversed splitting of second-heart sound.
• A fourth heart sound.
Pulse: A jerky carotid pulse with sharp upstroke (because of rapid ejection
and sudden obstruction to left ventricular outflow during systole).
JVP: prominent a wave due to forceful atrial contraction.

55. INVESTIGATIONS
X –ray chest: Heart usually not greatly enlarged
ECG:
• ECG demonstrates left ventricular hypertrophy
• Large abnormal Q waves in 20-50% of patients in leads II, III, aVF or V2-V6
(pseudoinfarction), lelt axis deviation.
• Occasionally LBBB OR RBBB, APCs, PVCs, short PR may be present.
Echocardiography: It is diagnostic showing:
• Asymmetric left ventricular hypertrophy.
• Systolic anterior motion (SAM) of anterior leaflet of mitral valve.
• Small left ventricular cavity size.
• Dilated left atrium.
• Left ventricular diastolic dysfunction.
Cardiac catheterization
• Small hypercontractile left ventricle
• Dynamic left ventricular outflow obstruction
• Diastolic dysfunction

56. RESTRICTIVE CARDIOMYOPATHY
• Restrictive cardiomyopathy is characterized by impaired
diastolic ventricular tilling due to stiffness of ventncIes with
preserved systolic contractile function. Because of the-
abnormallу elevated right atrial and ventricular filling
pressures, cardiac filling is diminished. As a result, the
clinical manifestations of restrictive cardiomyopathy usually
are predominantly right-sided. There is high atrial pressure
with atrial hypertrophy, dilatation and later atrial
fibrillation.
• Causes of restrictive cardiomyopathy
Amyloidosis, sarcoidosis, hemochromatosis
radiation, carcinoid syndrome, scleroderma,
myocardial fibrosis after open-heart surgery,
Loffler's syndrome.

57. • Symptoms:
1. Dyspnea and fatigue (due to low cardiac output).
2. Abdominal discomfort (due to hepatic congestion).
3. Restriction to ventricular filling results in persistently elevated venous
pressures and consequent hepatic enlargement, ascites and dependent
edema (right sided failure).
• Signs: Pgysical signs are simular to those of constrictive pericarditis e.g.
-Raised JVP with diastolic collapse (Friendreinch’ signs) and raised JVP on
inspiration (Kussmaul’ signs).
-Cardiac enlargement with a third or fourth heart sound is common.

58. Investigations:
• Chesty X-rays: It shows mild to moderate cardiomegaly.
• ECG: Usually has low-voltage, conduction abnormalities, ST
segment and T wave abnormalities.
• Echocardiography: It shows symmetrical myocardial
thickening,usually a normal systolic function, but impaired
ventricular filling.
• Cardiac catheterization: It shows higher diastolic pressure. Right
and left ventricular pressure tracings demonstrate a characteristic
"square root sign"—a deep and rapid early decline at the onset of
diastole followed by a rapid rise to a plateau. Normal or mildly
reduced left yentricular function.
Cardiac catheterization helps in distinction from constrictive
pericarditis.
• Endomyocardial biopsy: helpful in diagnosis

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Maneuvers

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Maneuvers

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Physical Exam in AS

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Echocardiography

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Physical Exam Review:

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Echocardiography

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Echocardiography

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Echocardiography

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Echocardiography

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Echocardiography

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Echocardiography

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Echocardiography