THERAPY FINAL EXAM QUESTION

CARDIOVASCULAR

1. RHEUMATIC FEVER

DEFINITION
a systemic immune D which occurs as a delayed sequel to pharyngeal infection with group A beta hemolytic
Streptococci which involves principally the connective tissues (heart, joints, CNS, skin, subQ tissue)

EPIDEMIOLOGY
For a variety of reasons, including wide availability of penicillin, the incidence of rheumatic fever in industrialised
countries declined dramatically between 1950 and 1980. In developing countries, however, where the spread of
bacterial infection is facilitated by poverty, limited access to healthcare and overcrowding, rheumatic fever and its
sequelae account for 25 to 40% of cardiac admissions to hospital. Outbreaks of rheumatic fever have also been
reported in developed nations, probably because of periodic reappearance of rheumatogenic strains of streptococci.

CLASSIFICATION
Acc to changes in heart
(1) Active phase
(a) Rheumocarditis w/o valve D
(b) Relapsing rheumocarditis (new process at places of old valve disorders)
(c) Rheumatic fvr w/o heart changes
(2) Non active phase
(a) myocardiosclerosis
(b) valve disorders
(c) changes in other organs (chorea, nephritis, hepatitis, changes in skin, encephalitis, meningitis)

Acc to duration
(a) Acute – acute beginning, attack duration b4 2 mths, presence of exudates, good & absolute effect fr treatmt
(b) Subacute – slow attack, 3-6 mths, has exudation, 1 or 2 degress of activities, X absolute effect fr Tx & X
rapid
(c) Relapsing - > dangerous, attack acute (6-12 mths), has exudation, 3rd degree of activity, X good effect fr Tx
(d) Long – slow attack, duration (6-12 mths), X exudation, 1’ or 2’ activity, some effect fr Tx but X good.
(e) Latent – X clinical, X lab changes but has valve disorders, 3’ activity
Max/3’ activity :
1. bright clinic : fever, polysyndromic changes
2. WBC >10
3. ESR > 40
4. fibrinogen>9
5. α2 globulin > 17
6. γ globulin >23
7. seromucoid >0.6
8. ASLO>3-5X more than normal

ETIOLOGY (ROLE OF HEMOLYTIC STREPTOCOCCUS). PATHOGENESIS

1 Hemolytic Streptococcus group A – widespread in environmt – causes upper respiratory Ds (pharyngitis,

sinusitis)
2 Normally attack in childhood 0.2-0.3% sufferers fr Strepto group A suffer fr Rh systemic D
3 Patho: When a susceptible host encounters a group A streptococcus, an autoimmune reaction results, which
leads to
4 damage to human tissues as a result of cross-reactivity between epitopes on the organism and the host (Fig.
5 322-2). Cross-reactive epitopes are present in the streptococcal M protein and the N-acetylglucosamine of
6 group A streptococcal carbohydrate and are immunologically similar to molecules in human myosin,
7 tropomyosin, keratin, actin, laminin, vimentin, and N-acetylglucosamine
MECHS :
 1. Streptococci produce enzs (Streptolysin, Streptokinase, Neurominidase, Protease)
3 Enzs → lesion of cell m’brane → destabilization of lysosome in cell → activation of intracellular proteases
→ damage of tissue when there is colony of MO in throat
2. Destabilizatn of basophils (e.g. Streptokinase activates it) → degranulatn→ BAS (Bradykinin, serotonin,
histamine) → inflmtory reactivation (vssl tone, mobility of vssls) → inflmtory rXn → direct harmful effect of tissue
4 Strepto has Ag (part of strepto cells → circulate in organism → immunosuppression
5 E.g. M prot → ↓ phagocytosis by neutrophils (suppress im rXn against bact)
6 If by genetic predisposition, has weak immune syst → harmful agent of Strepto
7 In ppl with genetically with properties of collagenic tissue who is not as stable in others
8 Soluble pt of collagenic complex (e.g. glucuronic acid) → Strepto enzs causes degradation of collagenic
complexes in wall of vssls in whole organism
9 Polysaccharides Ag react with cells of thymus → disbalance of T – B activity → after chronic Strepto
infection obtain sensitivity of plasma cells to produce Abs → disbalance of humoral activity
10 Weak immunity + colony of Strepto in throat etc → sensibilization → superactivation of humoral immunity
→ high Ab against Strepto → systemic collagenic D → chronic D → systemic collagenic inflmtory pathogenic D
(Rheu D)
11 Ag of Strepto has similar strucs to Ag of CVS of man (e.g. endothelial layer of myocardium etc → cross
rXn → Ab has tropism (affinity) to CVS Ag (e.g heart wall) → proteolytic activity of Strepto → self Ag release in
blood → autoim due to autoAb → attack working cells of CVS (but not as severe as SLE etc)

3. Delayed type of hypersensitivity → superactivatn of tissue lymphocytes (T-killers etc) → attack against
heart tissue → inside tissue deeply → rXn takes a long time (days & wks) → T lymphocytes may survive for
yrs (10-15 yrs) having memory of Strepto infection → recurrent episodes
12 When any non specific ↓ of immune homeostasis e.g. cold, stress etc → may result in activation of Strepto
somewhere localized e.g. pharyngitis, tonsillitis → Ab in blood
13 effect will be systemic attack CT e.g. heart valves (endocardium), eyes, etc
Factors that lead to Strepto attack:
1. Strepto infection
2. weak immunity
3. chronic (Strepto Ag ↑ by time to time)
4. Ag irritates humoral immunity
5. Sensibilization

3 main mechs of aggressive of Streptococci :

1. cross Ab structure of heart mm with Streptococci
2. aggressive activity of enzymes
3. activation of BAS

MORPHOLOGICAL STAGES OF RHEUMATIC DISEASE

Morphological changes :
Bact + Abs with proteolytic system of complemt → damage tissue → 2’ inflmtn → (↑ permeability & ↑ hydrostatic
P) due to collagenic degeneration/vasculitis → serum effusion inflmtn (at 1 st reversible) – reabsorbed if there is anti
inflmtory activity (4 wks till 2 mths) → ↑ permeability, constant destabilization of b/vssls walls → serofibrotic
effusion → coagulation of fibrin outside b/vssls (irreversible) → damage + necrosis of tissue (microscopic) → 2’
rXn of proliferation → superactivation of cells in area → accum of mononuclear cells → cell elemts of collagenic
tissue surrounds the area & isolate it fr non necrotized areas (Aschoff bodies) -2 mths → X blood supply →
degradation & proteolysis of cells → 2 nd wave of necrosis in Aschoff bodies → scarring + shrinking/ deformation of
inflamed tissue → recovering fr initial inflmtn

Morpho markers : Aschoff bodies

1 Stage 1 : Period of exudation (duration : 2 mths, if adequate diagnosis & treatment – may stop RhFvr
without complications to heart & lungs)
2 Stage 2 : Cells infiltration
3 Stage 3 : Sclerotic organic changes
CLASSIFICATION (acc to changes of heart – depends on active/non active phase)
(I) Active phase (II) Non active phase
1. Rheumacarditis without valve disorders 1. Myocardial sclerosis
2. Relapsing rheumacarditis – new active process 2. Valve disorders (many)
at place of old valve disorders 3. Polyarthritis, chorea, encephalitis,
3. RhFvr without heart changes meningoencephalitis, hepatitis, gomerulonephritis

DUKKET-JONES CRITERIA (2 major/1 major + 2 minor manifestations)

MAJOR MANIFESTATIONS MINOR MANIFESTATIONS

1. Rheumacarditis 1. temperature rXn – inflmtory D – febrile/subfebrile
2. Polyarthritis 2. weakness, malaise
3. Chorea of Sydenhem 3. perspiration
4. Erythema marginatum – vasculitis of skin 4. Arthralgia
o1 Transient pink rash 5. paleness - vasculitis
o2 Ring-shaped patches 6. Abdomen syndrome – with acute attack of Rh D → due to
o3 Subcutaneous nodules vasculitis → similar to peritonitis
5. Rheumatic anamnesis 7. Epistaxis – vasculitis in CNS
6. Exjuvantibus → aspirin treatment is good for
Rheumatic D & not for other collagenic Ds.
Plus (to minor criteria)
 supporting evidence of preceeding Streptococcal infection
 Recent scarlet fever
 ↑ed antistreptolysin O/other Strepto Ab titer
 (+ve) throat culture
 N.B : Evidence of recent Strepto infection is particularly important if there is only 1 major manifestation.
 Doppler U/S – mitral/aortic regurgitation (prolonged for 1 week)

CLINICAL PICTURE: SYMPTOMS OF PRIMARY & RECURRENT RHEUMOCARDITIS

Majority attacks in childhood are hyperergic in nature (cross rXn)
1) fvr 2) malaise 3) weakness 4) joints, skin changes 5) pancarditis etc
In adult, there’s delayed allergy & autoim Ab & no clear clinical pic

(1) Rheumocarditis
1 changes in endocardium (valve disorders) & myocardium
2 Myocarditis
1. soft heart tones
2. enlarged heart borders
3. systolic functional murmur above mitral valve
4. S3, S4, gallop rhythm devmt
5. heart insufficiency – dyspnea, fatigue, edema
 Signs of rheumocarditis
2. Heart murmurs if at 1st, heart is normal - suddenly in few days murmurs (due to edema & thickening →
valve dysfunction → sound of b/flow either systolic/diastolic murmurs)
3. If heart murmurs initially present, new onset of murmurs/changes of old murmurs
4. Dilatation of heart chambers
5. Quick devmt + progressing of heart failure (normally total failure, usually congestn of R side than L side of
heart, when there is proper treatment, can disappear total failure)
6. Pericardial effusion – very quickly dev → pericarditis devmt
6. Inflmtory edema → prob of conduction → 1st AV block (↑ PQ>0.2 sec)
If treat in time, no morpho changes, if not, changes in valves (50-60%)
Thickening of cusps & slight scarring
If has recurrent attacks, probability of valve D
After 2nd time, increase 95% cases has valve incompetence
If 3rd attack, 100% valve changes (75% mitral valve, 25% aortic valve)
Firstly
1) formation of commissures (1st time) – 2/3rds of ptt has Mitral stenosis, atrial fib
2) 2nd time – dev incompetence (shrinking & coalescence)
3) Aortic & other valve D – after many recurrent attacks

(2) Arthritis
 In young ppl, polyarthritis, large joints (knees, elbow, ankles), visible charac of inflmtn (defiguration,
edematous, skin pink & hot, pain (upon palpation or spontaneous)
 May dev rapidly & has migrating character, respond to treatmt
 In adult, normally is arthralgia

(3) Chorea
1 For young ppl
2 Can’t control mimic mm & extremities
3 Hyperkinetic activity of joints
4 Vasculitis of d
5 Responds to treatmt

(4) Skin changes

1 In young (allergy)

(5) Kidneys
2 Attack of nephrons causes 2’ glomerulonephritis (rheumatic)
3 Changes of urine (hematuria, proteinuria)

(6) Liver
1 Reactive hepatitis

(7) Changes in eyes

(8) Meningitis, encephalitis

RESULTS OF LABORATORY INVESTIGATIONS

Non specific lab tests :
1 throat swab culture for Streptococcal infection
2 Ab tests for preceeding Strepto infection (Strepto Ab titers differentiate preceeding streptococcal fr other acute
respiratory infections)
1. Antistreptolysin O - ↑ed titers (best) – standardized Streptococcal Ab test
2. Anti DNAse B/antihyaluronidase, anti Streptokinase
3. Antistreptozyme test – hemagglutination rXn to a concentrate of extracellular streptococcal Ags absorbed
to RBC
 ↑ed ESR, leukocytosis, may be anemia (suppression of erythropoiesis characteristic of chronic inflmtory Ds),
dysproteinemia (α- & γ-globulins), hyperfibrinogenemia
 ↑ed CRP (mucoprots, seromucoid, α-2, γ-globulins (biochem test)

U/S : changes in heart – thickening of valve leaflets, endocarditis, liquid in endocardium bed, heart size & chambers
enlargemt, hemodynamics data.
CXR : heart shape, lung state (pneumonitis, pleural effusion)
Urine analysis : ↓ specific gravity, hyaline cast, microhematuria, check kidney activity.

DIFFERENTIAL DIAGNOSIS OF BACTERIAL ENDOCARDITIS

TREATMENT: ANTIBIOTICS, NSAIDs, INDICATIONS TO CORTICOSTEROID THERAPY

Antidystrophic
NSAIDs Salicylates GCC Immunoactivators
drugs
 Indomethacin 25mg,    Mild immunodepressive
3X/day grp - Quinolines e.g. Delagil,
 Butadione Aspirin Prednisolone Parquinil
 Rheopirine large dose 20-30mg/day  For severe cases :
SE : blood productn depresn (<5g/day)  In - Imuram/Azathioprine
Therefore do blood analysis  SE : vasculitis (very
2X/wk for control ulceration active process)
 3rd degree
of activity

ANTIBIOTICS
Penicillin is the drug of choice and can be given orally [as phenoxymethyl penicillin, 500
mg (250 mg for children 27 kg) PO twice daily, or amoxicillin 50 mg/kg (max 1 g) daily, for 10 days] or as a
single dose of 1.2 million units (600,000 units for children 27 kg) IM benzathine penicillin G.

SALICYLATES AND NSAIDS

Aspirin is the drug of choice. An initial dose of 80
–100 mg/kg per day in children (4–8 g/d in adults) in 4–5 divided doses is often needed for the first few days
up to 2 weeks.
Glucocorticoids
prednisone or prednisolone are
recommended at doses of 1–2 mg/kg per day (maximum, 80 mg).

Management :
1. Atb – eradicate or inhibit Strepto – Penicillin (10-14 days), erythromycin
2. NSAIDs (1-1.5 mths), Indomethacin, ibuprofen, Ketoprofen, Butadione, Reopirin
3. If X effect fr both of in children, stop it abruptly. Use Hormonal remedies (glucocorticoids – prednisolone 20-
30mg/day in very acute process) + cytostatics (6-mercaptopurine, azathioprine)
4. Antimalarial drugs – only indicated in chronic D/recurrent attacks (age 30-40)
5. Metabolic agents – prevent dystrophy & scarring of heart e.g. Polyvitamins to improve metabolic of inflmted
myocytes
6. Additional : syndromic group by necessity
- in heart failure : diuretics, glycosides, VDtors etc, antiarrhythmic drugs
7. Prophylaxis
(a) avoid events of superactivation of im syst – use Atbs Penicillin with prolonged effects – frequent injection of
Bicillin 5
(b) Seasonal prophylaxis – spring + autumn when immunity is decreased- use anti inflmtory remedies for 1 mth to
avoid
inflmtory rXn

PROPHYLAXIS
1’ - prevent appearance of RhFvr i.e. treat laryngitis for 7 days effectively & prophylaxis of ptts & ppl near them
2’ - prevent relapsing of RhFvr :
 (a) seasonal – especially during autumn & spring (b) whole year - with Bicillin 5 (once a month)

2. INFECTIVE ENDOCARDITIS

ETIOLOGY
- 2/3 of the cases are caused by Gram +ve & -ve bacterias.
- Streptococci Viridans causes 30-70% of cases, Staphylococcus causes 10-30%, Enterococci causes more than 10%.
- Also causes by Gram –ve Klebsiella, E-Coli. Ricketsiae, Mycoplasm, Viruses, Fungi & Chlamydia also causes the
disease.

PATHOGENESIS
- Pathogenesis depends whether its :
a.) Primary disease : Heart is not diseased.
b.) Secondary : When presence of disease of heart such as Rheumatic disease, systemic collagenic disease, diseases
of valves, artherosclerosis of old people.
- It also depends on another classification of disease : Acute or Subacute or Chronic.
- In acute development, there is presence definite place from bacteria appearance in body (from injury, puncture or
trauma point).
- Presence of bacterial toxical effect & damage of heart by primary bacterial aggression which causes the lesion of
heart. This can cause increased endotoxicosis.
- 1st target of bacteria is the aortic valve (cusps) because in the aortic area, hemodynamics blood flow is most
intensive. So, bacteria that flow in blood adhere here & colonize the aortic valve.
- At end of 1st month of pathology, there is perforation of cusps. Main patho of affected valve is incompetency.
- Pyogenic Streptococci can cause acute depression of immunity in short period of time; so disease can increase
mortality.
- In subacute development, it occurs in :
i.) People who have some aortic valve pathology.
ii.) People who connected with early serious patho of heart such as rheumatic disease..(mitral valve patho is 2/3 of
all cases).
- So, problem appearance (lesion) in leaflets of mitral valve. Bacteria is transient (appear & disappear) in subacute.
Immunity/Treatment can reduce level of bacteria.a
- Bacteria localizes on surface of cusps & produces proteolytic enzymes causing injury of cells. This causes
infiltration of more mononuclear cells (proteolytic substances) damaging bacteria & also own heart cells.
- Next, there will be edema of valves & cusps become thicker; finally appears necrosis.
- There is proliferation of cells in cusp area : Epithelial cells from collagenic fibers & appearance of
polyps/vegetations at affected cusps. They work like berry.
- Presence of BAS that stimulates hypercoagulation causing thrombi formation on affected cusp of valve. This
causes dysfunction of valve because its badly closed. This may result in heart failure.
- Duration life of vegetation longer on cusp. Here, presence of stenotic changes. Later, vegetation can be broken
causing incompetence.
- Surface of vegetation filled by thrombi, risk of thromboembolic increase.
- In chronic, there can be chronically impaired immunity connected with reduced production of complement.
- Cells are distributed to different part of vascular system. Complexes are absorped on vessels of kidney & velocity
of filtration decrease. Also in liver, synovial joints which can cause immune complex vasculitis.

CLINICAL PICTURE
- Its divided acc :
i.) Acute :
- Its recurrent.
- There are increased perspiration, serious weakness, anorexia, sleeplessness, ↑ temperature more than 39degrees,
loose weight more than 10kg in 1-2weeks.
- There are also muscle dystrophy, hypovolemia with tachycardia, anemia (end of 1 st week), dev damage of valve
structure in 10days-2weeks, wide spread abscess, aggressive thromboembolism (pulmonary artery, coronary sys).
- Patient can survive.

ii.) Subacute :
- Ppl don’t remember the onset.
- Onset : Cold, simple disease symptom such as weakness, malaise, headache, sweat is common, subfebrile reaction
that takes 1-2months without changes.
- After 2-3weeks, there is inflammatory syndrome same as in acute but not serious : ↑ temperature to high level then
drop to subfebrile level, loose weight, colour skin change : Coffee with milk (blood not sterile), depression of
adrenal gland activity.
- Presence of clubbed fingers, presence hepatolienal syndrome (splenomegaly), disease of liver cirrhosis, disease of
blood.
- Presence of inspiratory dyspnoe, palpitation, enlarged heart shape, presence of murmurs that’s appear new/old
which become louder; become systolic & diastolic murmur.
- Vascular patho : Embolism & toxical vasculitis, myocarditis (enlarged heart by edema), pericarditis (pain in
substernal area) with formation of liquid & exarcebate heart failure, coronary syndrome (embolism to coronary
vessels).
- Petechial rush/HR in chest; presence of spots HR in sclera & conjuctiva.
- Systemic immune vasculitis : Causes secondary glomerularnephritis & HT. Changes urine : Hematuria.
- Presence of vasculitis on skin : Osler’s Nodules in palm, soles (0.5-1cm diameter). They are painful, red colour,
protruded outside the skin.
- Systemic vasculitis in liver with toxic effect & hepatitis causing hepatomegaly.
- Presence of thrombosis of pulmonary artery with necrosis, infarction of lung. Can have pneumonitis.
- Toxicity with depression of bone marrow : deep, hyporegenerative anemia, lymphopenia, plasmocytosis.

INVESTIGATION
i.) Blood :
- Hyporegenerative anemia, thrombocytopenia.
- Leucocytosis at onset of disease, paradoxical leucopenia, shift to the left : Appear band leucocytes.
- Aneosinophilia symptomatic for whole period of disease.
- ↑ ESR (60-80).
- Plasmacytosis appear in blood. Can find causative factors in blood culture.
ii.) Biochemical :
- Dysproteinaemia : Appear alpha2-globulinaemia.
- Presence of transient azotemia
iii.) Urine :
- Proteinuria, hematuria, leucocyturia : Toxic kidney/glomerularnephritis.
- Presence bacteria in blood : Not sterile.
* Must do test before systemic A’biotics therapy; blood test done at ↑ temperature (from venous & arterial system).
At least 5 samples puncture vessels done to obtain blood. If at least 2 times has +ve results, disease is confirmed.
- Must check immunity by immunogram : ↑ level of Ig G & Ig M.
iv.) Instrumental :
4 US : Show bacteria situated in valve. It shows vegetations because they are large. It also shows cond of chambers
(size,etc).
5 ECG : Changes in electrical activity of heart.
6 Radiology : show cond heart, congestion at lungs.
* Must do US of spleen, kidney…
Results :
- Heart affected 100%; infarction due to embolism : 5-15%, abscess of heart rare; brain affected in 30%
(encephalitis, mycotic aneurysm..), kidney 30-50% (toxical kidney).
- Joints (synovial changes) is 25-30%, spleen enlarged 90%, thromboembolic syndrome & HR in 80% cases.

TREATMENT (ROLE OF ANTIBIOTICS)

i.) Antibacterial/Antiinfective Remedy :
- AB therapy at max dose : Penicillin (IV 20million in subacute; 60-80million in acute). If mix flora, do combination
therapy with A’glycoside (Gentamycin/Tobramycin) 3times/day; IV.
- Also can use Monolactam AB : Tionam 1-2g/day IV. If known flora such as Staphylococci, use last gen Penicillin :
beta lactam, Amoxycoclaf. Can plus with Vancomycin/Cephalosporins of 3rd – 4th gen & Lincomycin.
- Enterococci : Vancomycin + Cephalosporins.
- Can use Ampicillin 2g, IV 6times/day; Pepericillin 3g IV every 4 hours; Vancomycin 15mg/kg 2times/day;
Tobramycin 1.7mg/kg 2times/day.
- Gram –ve : Cephalosporins (3rd & 4th gen), A’glycoside last gen, Monolactam AB.

ii.) IV intake of Antiseptics : Dexidin 100-500ml/day.

iii.) Remedy for immunity : Polyvalent gamma-globulin. If not effective, use Cephalosporin last gen; IV Colfracan
4-6g; Cephalosporins with A’glycosides or Quinolones.
.- Fungi : Diflucan, Ketokenazole, Fungisone IV.
- Antivirus : Cicloferon, Foskarnet.
- If treatment not enough in 6weeks, must do surgery. Resection of valve & do prothesis. The next AB therapy will
be better. * Use AB Fluoroquinolone before minor surgery.

3. MITRAL STENOSIS

ETIOLOGY
- Most common cause is rheumatic valvular heart disease (with rheumatic fever & chorea).
- Lutembacher’s syndrome, which is the combination of acquired mitral stenosis & an atrial septal defect.
- A rare form of congenital mitral stenosis.
- In the elderly, a syndrome similar to mitral stenosis, which develops because of calcification & fibrosis of the
valve, valve ring & subvalvular apparatus (chordae tendinae).
- Carcinoid tumors metastasizing to the lung or primary bronchiol carcinoid.

HEMODINAMICS ABNORMALITIES
- The atrioventricular orifice narrows due to the adhesion of mitral cusps, their consolidation & thickening &
shortening of tendons. Valve becomes funnel shaped with a narrow slit in the middle.
- Stenosis is significant : (normal 4.5cm2 to 1.5cm2).
- In diastole, blood fails to enter left ventricle fr left atrium; so the remaining blood + additional blood coming from
pulmonary veins overfills left atrum with blood & ↑ pressure.
- ↑ pressure is 1st compensated by ↑ atrium contraction & causes its hypertrophy. Soon, there will be weakened
contractile force causing the atrium to be dilated & ↑ pressure. This ↑ pressure in pulm veins.
- Arteriole spasm occurs in the lesser circulation (Kitaev’s Rx) & ↑ pressure in pulm A.
- So, right ventricle works harder to overcome pressure in Pulm A & becomes hypertrophied too. This leads to
systemic congestion.
- Left ventricle slightly reduces in size due to the lesser amount of blood entering it & so, lesser activity.

CLINICAL PICTURE
- Cough can be with blood & rales. Effort related dyspnoe.
- Breathlessness, fatigue, chest pain, ascites & edema in legs in severe degree of diseae.
- Can have mitral face, small character of pulse & rapid which is different at both hands due to compression of
artery at hypertrophy of left ventricle.
- Ortner’s sign (hoarseness) : Recurrent laryngeal nerve compression by dilated left atrium.
- May have dilation of neck veins.
- Presence of epigastric pulsation due to hypertophy of right ventricle.
- Atrial fibrillation can reduce cardiac beat (less left ventricle movement).

INVESTIGATION (ECG, ULTRASOUND, X-RAY)

i.) ECG :
- P-Mitrale (left atrial hypertrophy).
- Broad negative phase of diphasic P in V1 or atrial fibrillation of ‘f’ waves.
- Right ventricular hypertrophy. In pulmonary hypertension : tall peaked P waves in lead II & upright in lead V1,
right axis deviation, right ventricular hypertrophy.
ii.) US :
7 Can estimate transvalvular gradient & of mitral orifice size, the presence & severity of disease.
8 It also tells the extend of restriction of valve leaflets, their thickness, the degree of distortion of subvalvular
apparatus.
9 It also assess the size of cardiac chambers & estimation of left ventricular function.
iii.) X-Ray :
- Straightening of the left border of cardiac silhouette, prominence of main pulmonary arteries, dilatation of upper
lobe of pulmonary veins & backward displacement of the esophagus by an enlarged left atrium.
- In severe stenosis, all chambers & vessels upstream to the narrowed valve are prominent.
- Kerley B lines are fine, dense, opaque, horizontal lines that are most prominent in lower & midlung fields.

INDICATIONS FOR SURGICAL TREATMENT

- When presence of severe narrowing of the mitral valve.
- If pulmonary hypertension develops or the symptoms of pulmonary congestion persists despite adequate therapy.
- If develops complications such as severe atrial fibrillation, systemic embolization, right ventricular failure,
tricuspid regurgitation, etc.

4. MITRAL REGURGITATION.

ETIOLOGY
1 In acute rheumatic fever, mitral valve prolapse, myocarditis, dilated cardiomyopathy, hypertension, IHD,
infective endocarditis, hypertrophic cardiomyopathy, systemic lupus erythematosus, collagen disorders in Marfan’s
syndrome & as side effects of drugs usage such as fenfluramine.

HEMODINAMIC ABNORMALITIES
2 Mitral valve fails to close completely → blood is gurgitated to LA in systole → blood filling of atrium
increased (pressure increases- atrium dilates & development of hypertrophy) → increased blood volume delivered
to LV in diastole → LV works harder in systole due to increased blood volume in it → LV hypertrophy →
contractile power of LV weakens afeter some time → diastolic pressure increases → increased pressure in LA →
increased pressure in pulmonary veins → spasm of arterioles in lesser circulation( Kitaev’s reflex) → increased
pressure in pulmonary artery intensify load in RV ( contracts with more force to eject blood) → RV
hypertrophy.

CLINICAL PICTURE
3 Usually in the early stages patient has no complaints & looks healthy due to compensatory powers of the LV.
4 When there’s congestion of lesser circulation there’s gradual dyspnea development due to venous pulmonary
congestion & palpitation of heart develops due to increased stroke volume.
5 Fatigue due to low cardiac output & lethargy sets in. Pulse is of high volume & tachycardic & in later stages
might be irregular pulse due to atrial fibrillation. Jugular veins are dilated. Apex beat is localized & tapping.
6 In later stages might develop right heart failure with edema & ascites development.

INVESTIGATION (ECG, ULTRASOUND, X-RAY)

1 ECG- left atrial delay ( bifid P waves ) & left ventricular hypertrophy .
2 X ray- shows mitral configuration with displaced borders to left & superiorly ( LA & LV enlargement). In later
stages can see enlarged right side due to right ventricular hypertrophy.
3 Auscultation- systolic murmur above apex that radiates to left axillar & under left scapula. It arises systole & is
synchronous with S1. Soft S1 at apex due to absent valve component of 1 st tone. Accentuation of S2 at pulmonary
trunk due to pulmonary hypertension. Prominent S3 due to sudden rush of blood back into dilated left ventricle in
early diastole ( sometimes a short middiastolic flow murmur may follow).
4 PCG

PROGNOSIS

5. STENOSIS OF AORTIC VALVE.

ETIOLOGY
1 Arteriosclerosis, rheumatic fever, infective endocarditis. Also in can be congenital.

HEMODINAMICS ABNORMALITIES
2 During systole, LV is not emptied completely because portion of blood fails to pass the narrowed aortic valve into
the aorta.
3 When a new normal portion of blood is delivered into LV during diastole from LA it is mixed with the residual
volume & ventricle thus becomes overfilled.
4 The pressure in inside LV thus rises. This cause intensification of LV work thus it hypertrophies as a
compensatory mechanism.

CLINICAL PICTURE
1 Can be asymptomatic for many years due to the compensatory mech of LV.
2 If obstruction in orifice is considerable, insufficient bllod ejection into arterial system upsets normal blood
supply to hypertrophied myocardium & patient feels angina like pain in physical exercise & emotional stress.
3 Aortic face-pale.
4 Giddiness, headache, tendency to faint ( exertional syncope) due to disordered blood supply to brain.
5 Exertional dyspnea. Episodes of acute pulmonary edema.
6 Small slow pulse. Enlarged apex beat & displaced to left. Deformation of chest if problems develop at young.
7 In palpation can feel systolic murmur ( cat’s purr).

INVESTIGATION
1 ECG- signs of LV hypertrophy & sometimes coronary insufficiency. ST changes ( doen sloping ST segment &
T inversion), LBBB. ECG can be normal even in severe stenosis.
2 X ray- aortic configuration of heart with LV hypertrophy & post stenotic dilatation of ascending aorta.
3 Auscultation- at apex, dimished S1 due to over filling of LV & prolongation of systole. S2 diminished over
aorta & can be inaudible of aortic cusps adhere & are immobile. Rough systolic murmur over aorta & is heard when
patients sit in 2nd ICS. Murmur is conducted by blood into carotids & can be heard in the interscapular space & in
the neck. This murmur is an ejection systolic murmur that is of crescendo-decrescendo type.
4 US- in US we measure the diameter of the aortic valve orifice. In soft degree it’s 1.2-2cm square, moderate it’s
0.75-1.2 cm square & severe is less than 0.75 cm square.
5 PCG
6. AORTIC VALVE REGURGITATION.

ETIOLOGY
Acquired
1. rheumatic disease(inflammatory & sclerotic changes occur in the base of cusps causing it to shrink &
shorten)
2. infective endocarditis
3. trauma
4. aortic dilatation (Marfan’s syndrome, syphilis, aneurysm, dissection, ankylosing spondylitis)
Congenital
1. bicuspid valve or disproportionate cusps

HEMODINAMICS ABNORMALITIES
1 Aortic incompetence is the failure of the aortic valve to close completely during ventricular diastole→
blood leaks back into the left ventricle.
2 During diastole→blood delivered fr left atrium & also fr aorta due to regurgitatn→overfills & distends L
vent in diastole→in systole, left vent contract with >er force to expel larger blood vol into aorta→L vent
hypertrophied due to intensified work & ↑ed systolic P in aorta causes its dilatation.
3 There is a marked variation of BP in aorta during systole & diastole. Increased blood vol in aorta at systole
↑es systolic P & part of blood returned to vent at diastole causes diastolic P to↓.

CLINICAL PICTURE
1 Until onset of breathlessness : awareness of heart beat (on left side)
2 Paroxysmal nocturnal dyspnoe
3 Tachycardia, dyspnea, weakness- <er circ congestion
4 Giddiness-deranged b/supply to brain
5 Pallid skin- insufficient filling of arterial system during diastole
6 Aortic face
7 Dancing man- Musset sign : head nodding in sagittal position
8 Landolfi- pupil pulsation
9 Peripheral aa pulsation- carotid shudder, subclavian, brachial, temporal.
10 Quinke’s pulse- capillary pulsation in nail beds
11 Durozeiz’s sign – femoral bruit.

INVESTIGATION
1 Palpation- enlargement & shifting of apex beat to the left & inferiorly (6th or 7th hypochondrium)
o Apex beat is diffuse, intense & rising like a dome.
2 Percussion- border of cardiac dulless- shifted to left, heart is aortic with pronounced waist.
3 Auscultatn- Soft both heart sounds.
o diastolic murmur above aorta at Botkin Erb point (better aus in deep breathing)
o relative mitral valve incompetence- there is systolic murmur due to regurgitation.
o Austin Flint murmur- soft mid-diastolic murmur present
o 3rd & 4th sound may appear.
o Traube double sound heard over femoral aa
4 Pulse- fast , full & ↑.
5 X- ray- enlarged left ventricle,aortic dilatation, aortic configuration.
6 ECG- left ventricle hypertrophy
7 Echocardiogram- in aortic failure, can see flutter of anterior wall of mitral cusps during diastole due to thrust
of blood regurgitated fr aorta into vent.

7. TRICUSPID VALVE REGURGITATION

ETIOLOGY
1 Organic- due to rheum endocarditis
2 Functional- due to dilatation of R vent & distention of R atrioventricular orifice.Often combines with mitral
stenosis bcoz RV perform >er work due to High P in <er circ.

HEMODYNAMICS ABNORMALITIES
1 Due to incomplete closure of the tricuspid valve during the RV systole→part of blood regurgitated into R
atrium→mixed with normal blood delivered fr vena cava→atrium bcomes distended & hypertrophied.
2 During diastole→larger blood vol delivered into RV →causes dilatation & hypertrophy of RV.
3 Compensation in this disease is by intensified work of R atrium & RV which compensatory power is not great
so congestion in greatr circ develop.

CLINICAL PICTURE
1 Feeling of heaviness
2 Pain in the right hypochondrium
3 Edema, ascites
4 Skin bcomes cyanotic , sometimes with yellowish tint.
5 Neck veins swells & pulsates.
6 Pulsation of liver; positive venous pulse.

INVESTIGATION
1 Inspection- pronounced pulsation in region of RV (systolic retractn & diastolic protrusion)
o Sys retractn- due to pronounced diminution of RV blood bcoa its elivered to hepatic veins. (systolic
swelling of liver)
o Diastolic protrusion- diastolic overfilling of RV & protrusion of chest in ventricular region + diastolic
diminution of liver vol.
2 Palpation- Specific rolling movements when place one hand on liver & the other on RV region.
o Liver displaced anteriorly & swell- hold liver by both hands, pulsating liver sets the hand apart during
the pulse wave.
o apex beat not pronounced bcoz displaced postly by hypertrophified RV.
3 Percussion- marked displacement of the heart border to the right fue to hypertrophy of Right atrium & ventricle
4 Auscultation- at base of xiphoid process- diminished 1st sound
o Systolic murmur at xiphoid process & at 3 rd &4th interspace, to R of sternum- murmur increase when
 patient keep his breath at height of inspiration
o 2nd sound over pulm trunk ↓.
5 ECG : hypertrophy of RV (electrical axis shift to R).
6 PCG: systolic murmur at base of xiphoid pro & at 3 rd & 4th intercostals space to the R of sternum, systolic
murmur has↓ing character
7 X ray: hypertrophy of right chambers.
8 Phlebogram of jugular veins : high +ve a wave which is connected with the intensified activity of
hypertrophied right atrium. (or form characteristic of +ve venous pulse)

8. CHRONIC HEART FAILURE

ETIOLOGY
1 All diseases of the heart
2 Primary causes : IHD, MI, myocarditis, sclerosis (post MI)
3 Secondary causes :
(a) Problem with pressure/ ↑ preload
- arterial HPT (essential )
- 2° arterial HPT
- pulmo HPT
- stenosis of aorta
- mitral stenosis
(b) Problem with volume
- insuff of aorta
- insuff of mitral valve

PATHOGENESIS
1) Small cardiac output
2) ↓ contractility of cardiac muscle
3) Activation of sympathetic system
- spasm of a.a & v.v
- tachycardia develop
4) Small bf in kidney (ischemia )
5) Activation of renin AT converting system
- activation of a.a & v.v
6) Activation of Aldosterone system
- improve reabsorption of Na+ & H2O
- a.a.r enlargement of circulation blood
- dilatation of heart chambers
- small output
- ↓ contractibility of cardiac muscles

CLASSIFICATION
1 Acc to Russian classification by Vasilenko:-
1) Stage I - at rest, absent insuff
- clinical feature only appear after physical exertion
( tachycardia, different arrhythmia, fatigue )
2) Stage II - present prob with 1 or 2 blood flows
Stage IIa - after adequate Tx, all changes disappear
Stage IIb - usually present changes in both bf after Tx
- cond improve but clinical features present
3) Stage III - sclerotic stage, cachexia dev & absent effect from Tx

2 According to American classification ( functional ) :-

1) Func I - no breathlessness
- normal physical activity
- without any changes
 - tachycardia, dyspnea maybe appear in normal physical exertion
2) Func II - at rest, absent features of heart insuff
- in physical exertion → dyspnea, tachycardia, fatigue
3) Func III - at rest, all symptoms absent
- in phy exertion → dyspnea, tachycardia, fatigue
4) Func IV - at rest, present features of heart insuff
- ↑ in minimal physical activity

CLINICAL SIGNS ACCORDING TO STAGES

** pls refer above **

TREATMENT: GLYCOSIDES, DIURETICS, VASODILATORS, ACE-INHIBITORS

(1) ß-blockers
3 Before Func II class only
4 For other stages, cannot use because can cause depression of the heart

(2) ACE- Inhibitors

1 Inhibit rennin angiotensis
2 Eg : Captorpil 25mg per day
Enalapril 10mg x 2 ( if ↓ bp : 2.5mg x 2 )
Periendopril 4-8 mg per day ( depend on bp )
1 S/E - ↑ dry cough
- hypokalaemia ( in serum )
- allergic reaction
- tachycardia
- bradycardia
- hypotension
- AV Block
- bronchospasm ( very dangerous )
- changes in mucous

(3) Glycosides
2 Most common are : Digoxin, Digitoxin, Strophantin
3 Strophantin or Corticone - short time activity
- polar drug
- in acute situation only
- can dev edema of lungs, diff type of arrythmias
- rapid effect in short time
- mostly by IV
- no cummulation
1 Digitoxin - for chronic situation
- got cummulation ( very high )
- MOA → increase contractility (positive inotropic effect )
→ edema disappear
→ bradycardia dev if tachycardia before treatment
→ Normalization of extrasystole
→ enlargement of diuresis
→ normalization of HR
→ improvement condition of pt
Glycosides
2 Contraindicated in - acute MI
- bradycardia ( different AV block )
- aneurysm of the heart
- obstructed myocardiopathy
 - WPW syndrome
- Ventricular tachycardia
3 Overdosage - can cause heart to stop
- sensitivity of org to glycosides are different. Thus different scheme of Tx
4 Intoxication - development of extrabeat ( ventricular tachycardia bigeminy & trigeminy )
- ↓ appetite ( dyspectic ) : nausea, vomiting, discomfort in epigastric region
- yellow greenish vision
- ↓ K+, L.O.C, hypokinesia, fatigue
- delirium which lead to development of psychosis
5 Antidotes → UNITOL ( chelate subs that contain antidote & will be excreted thru urine )
→ Ab can also be used ( combine & interact with glycosides )
6 Tx of overdose - withdrawal
- infusion K+ containing drugs ( IV )
- UNITOL ( antidotes )
- treat with dose ( ↓ 25 % ) of initial dose
- Ab for glycosides maybe used also
(4) Diuretics

(a) Thiazides
7 Eg : Hypothiazides ( 25-100mg/d )
8 Cyclomethiazines ( 0.5-1.5mg/d )
9 S/E : hypokalemia, ↑ Ca2+ level, dysfunction in glucose changes
10 Specific of activity : absent effect in case of renal insuff as diuretics effect lower than furosemide
11 Activity begin 1-2 hours after intake in 12 hours

(b) Furosemides
1 More intensive
2 Rapid, good, short effects
3 Therapeutic dose : 40mg/day in the morning
4 Max dose : 2mg ( incase acute renal insuff )
5 In cardiac pt, acute dose max 60-120mg/day ( IV )
6 S/E : losing K+ → so use with K+ containing drugs ( aspartame & panalgine )
: can use in combination with spironolactone
: thrombocytopenia, hyperuricemia, metabolic relapsing arthritis
: hearing prob ( short time )
: Furosemide depending renal syndrome dev in prolong usage ( kidney cant work w/o
Furosemide )

(c) Spironolactone
1 Eg : Veroshspirone ( 0.25mg 1 tablet with combination to other drugs )
Max is 2-12 tablets per day
2 Resistance to heart insufficiency or liver cirrhosis
3 Eg : Triamterine ( 50mg )
Amiloride ( 5 mg )
1 S/E : hyperkalemia, changes in lipid metabolism
2 C/I : renal insufficiency

Scheme for treatment of Glycosides

a) Rapid – max dose which correct condition of pt inject in 1 day
b) Moderate - main dose : 3 days
- slower scheme

Scheme for treatment of Diuretics

1 Begin treatment if edema develop
2 Starting with Thiazide diuretics
3 Maybe use combination if present heart insuff
4 Decrease level of salt & water

Scheme for treatment of Vasodilators

1 Independ of place :-
a) Direct → eg: Nitrous, Sodium Nitroprusside, Minixidil
b) Ca2+ antagonist
c) ά-adrenergic blockers→ eg: Filtolamin, Prazosin
d) Antagonist for K+ channels → nicoradine
 Depending of places :-
a) Veins → nitrous, morsidimine, cardatum ( ↓ preload & relaxation of veins )
b) Arteries → Ca2+ antagonist eg: eprosine ( relaxation of arteries & ↓ afterload )
e) Mixed → ά-adrenergic blockers, Ca2+ antagonist ( nitroprusside )

Surgical treatment
1 Transplantation of heart

9. ACUTE HEART FAILURE

ETIOLOGY
2 Primary causes → IHD, MI, Myocarditis, Sclerosis
3 Abnormal preload → aortic valve insufficiency & mitral valve insufficiency
4 ↑ afterload → stenosis of the aorta, arterial HPT (1° & 2°)

TYPES
1 Right & left
2 Systolic & diastolic
3 Low output & high output
4 Forwards & backward

PATHOGENESIS
a) Small cardiac output
b) ↓ contractility of the cardiac muscle
c) Activation of sympathetic nervous system
1 Spasm of a.a & v.v
2 Tachycardia development
d) Small bf in the kidney (ischemia)
e) Activation of the renin angiotensin converting system → spasm of a.a & v.v
f) Aldosteron system activation
 Improve reabsorption of Na+ & H2O
 a.a.r enlargement circulation blood
 dilatation chambers of the heart
 small output
 ↓ contractility of the cardiac muscle

CLINICAL SYMPTOMS
1 Cardiac asthma
2 Orthopnea
3 Mixed dyspnea
4 Acrocyanosis
5 Moist rales
6 Sputum pink color due to diapedesis of the erythrocytes

EMERGENCY CARE
1 Morphine
2 Diuretics
3 Nitrous
4 In ↑ arterial pressure : nitroprusside
5 In ↓ arterial pressure : prednisolone, mesathone
6 Cardiac glycosides

10. ATHEROSCLEROSIS

EPIDEMIOLOGY
Male > 45 160/90-95 or higher
Risk to atherosclerosis to IHD

ETIOLOGY – MODIFYING & NON MODIFYING RISK FACTORS

Modifying:
1. Drug taking to control hypertension
2. Smoking
3. DM type II
4. Hypodynamia
5. Obesity

Non modifying risk factors:

1. Hyperlipidemia or dyslipoproteinemia
2. CNS type A – more competitive and superactive
3. Sex
4. Age

ROLE OF DYSLIPOPROTEINEMIA
Forms: free fatty acids, cholesterol, triglycerides, esthers, phospholipids
Dyslipoproteidemia dev due to:
1 ↑ absorption fr GIT
2 Changes of receptor activity/ sensitivity
3 Transport systems affected
4 When cholesterol is not evacuated properly
Mech:
1. Initial damage to b.v.
2. Inhibition by lipids
3. Damage of cells
4. Stimulation of smooth muscles cells
5. Formation of atherous cap containing atherosclerotic debris

TYPES ACCORDING TO FREDRIKSON’S CLASSIFICATION

1. Hyperlipoproteinemia type I (lipoprotein-lipase deficicency) -↑ chylomicrons
2. Hypercholesterolemia types IIA and IIB
 IIA – only LDL↑ and ↑CLTRL
 IIB – ↑ LDL and VLDL ↑ CLTRL and ↑TG
3. Dysbetalipoproteinemia - ↑IDL→↑ LDL
4. Hypertriglyceridemia - ↑ VLDL
5. Hyperprelipoproteinemia - ↑ chylomicrons and ↑ VLDL

PATHOGENESIS
Dysplipoproteinemia→ lipids absorbed on endothelial cells of blood vessels→ primary injury to cells→ change in
permeability→ receptors activity↓→ cholesterol becomes depot in cell, block other cell activities e.g. metabolism→
dystrophy→ intima of blood vessel disappear→ basement membrane seen or exposed→ thrombosis covers defect, ↑
activity of smooth muscle cells (localized hypertrophy)→ intimal thickening→ formation of atherous cap containing
atherosclerotic debris
MORPHOLOGICAL STAGES OF ATHEROMA FORMATION
1. Fatty streaks – cells have many fat vacuoles (may be seen in childhood)
2. Intimal thickening (reversible)
3. Fibrous cap above muscle (fibrous plaque), may occlude lumen, if >90% infacrtion of tissue below supply.
4. Total scarring – destabilization of plaque, stress, physical activity etc break fibrous cap, contents rush out
cause stimulation of thrombocytes and form large thrombus→ infarction/ insult→ growth of collagenic fibres→
shrinking→ calcification (irreversible)

CLINICAL SYMPTOMS OF AORTA, BRAIN & PERIPHERAL ARTERIES ATHEROSCLEROSIS

1st place of atherosclerosis dev in ascending aorta
clinical syndromes: systolic isolated hypertension ( only ↑ systolic P), aorta lost elasticity due to calcification and
sclerosis ( systolic P not compensated), ↑ S2 in aorta – calcification of aortic valves or stenosis (systolic mumur in
aorta with rhomboid shape), dilation of aorta- aneurysm, thromboembolism – organ ischemia, aortic dissection.

2nd place – coronary system

IHD (acute coronary death, angina pectoris, MI, cardiosclerosis, heart failure→ arrhythmia

3rd place are brain arteries esply int and ext carotid arteries
Carotid ext – vascular hypertension
Int carotid artery – decirculative encephalopathy, ↓ memory, reflex, behaviour (chronic), acute case is insult

4th place – kidneys

↓ perfusion to renal arteries ↑ renin synthesis→ renovascular hypertension→ chronic renal failure
Or kidney infarction → acute renal failure

5th place- abdominal arteries – celiac trunk and brr

Abdominal angina after eating due to ↑ blood demand
Acute abdominal syndrome due to necrosis

6th place: Peripheral arteries – normally lower limbs

Trophic disorders

TREATMENT: DIET, MEDICAMENTS

Diet with high concentration of unsaturated fat, ↓ salt, 150mg CLTRL/ day, eggs 1 per week, milk 0.5% fats, vege,
fruits, seeds, nuts used each day, control sugar, sweets and butter.
Drugs to control:
1. Bile acid sequestrants ( block absorption of fats fr food by GIT): Questran, Quentalan, Cholestipol
2. Nicotinic acid derivatives (activates lipoprotein lipase thus ↑ing lipid metabolism): induracil, vitamin B
3. Fibraates ( ↑ HDL) – clofibrate, besofibrate, ciprofibrate
4. Probucol – block synthesis and CLTRL absorption
5. Statins* - inhibit HMG-CoA to ↓ CLTRL synthesis e.g. lovastatin, simvastatin, nevastatin
Combination therapy: group 1 and 5 or group 1,3 and 5 etc.

PROGNOSIS
The severity of atherosclerosis is closely associated with risk of myocardial infarction, cerebrovascular disease and
death from vascular causes; the reduction in risk factos is the most useful therapy
11. ISCHEMIC HEART DISEASE

DEFINITION
occurs when there is an imbal. btwn supply of O2 & myocardial demand

EPIDEMIOLOGY
In the 20th century:60 mill. Ppl/yr
Men:Women= 4:1
Before age 40 = 8:1
Aft age 70 = 1:1
ETIOLOGY
1) Coronary b.flow to a region of the myocardium may be ↓ by mech. Obstrucn :
atheroma,thrombosis,spasm,embolus,coronary stenosis,coronary arteritis in SLE
2) ↓ in flow of O2 blood to myocardium: anemia,HPT causing ↓ coronary perfusion P,
carboxyhaemoglobulinaemia
3) ↑ demand for O2 occur due to ↑ cardiac output ( thyrotoxicosis)/ myocardial hypertrophy (aortic
stenosis/HPT)
4) Abnorm constriction/failure of norm dilation of coronary resistance vessels
Risk factors : age, male sex, family history(gen.predisposition), diet high in fats, hyperlipidaemia,
smoking,stress,excessive alcohol intake, HPT,DM, obesity, lack exercise, gout, contraceptive
pills,homocysteinaemia,elevated non-spec. markers of inflamn-fibrinogen, C-reactive prot, ferritin, ↑LDL,↓HDL

PATHOGENESIS
1) Segmental AT narrowing of epicardial coronary arteries by plaque formation → fissuring,HR&thrombosis →
worsening obstrucn,coronary b.flow ↓ → myocardial ischemia
2) Disturbances of vascular endothelium func (local ctrl of vascular tone,maintenance of a/coagulant surf,defense
against inflamn cells) causes inappropriate constricn,luminal clot formation,abnorm interacn wit monocytes &
platelets
3) ↓ in luminal diameter of arteries( produces ↓in luminal cross-section area) causes hemodynamically significant
stenosis → smaller distal intramyocardial arteries &arterioles are max dilated → any ↑ in myocardial O2 demand
provokes ischemia

CLASSIFICATION ( not sure)

1) Acute : Angina pectoris, Myocardial infarcn, Sudden coronary death
Chronic : Diffuse /post-infarct cardiosclerosis
Arrythmia
Heart failure
2) Acc to location : Ant, Post, Lat,Interventricular wall, large(diffuse)
3) Acc to involvement of heart m : Subendocardial,transmural,intramural
4) Acc to duration : Transient ischemia(angina pectoris), Prolonged ischemia ( myocardial necrosis& scarring)

PRIMARY PROPHYLAXIS ( not sure)

- Ctrl diet,more exercise, ↓stress& avoidance of othr risk factors

12. ACUTE CORONARY DEATH

12 can live wit infarct for 3-5days then death due to reaction frm coronary artery due to thrombosis

ASYSTOLE

FIBRILLATION

TAMPONADE OF THE HEART

13 compression of the heart due to presence of accumn of effusion in the closed pericardium & it x distend
further, thus produce disturbances in circulation by preventing ventricular filling
14 features : ↑ jugular venous P wit sharp diastolic collapse,Friedreich’s sign(y descent),paradoxical
pulse,dilatation of neck veins during insp. (Kussmaul’s sign), ↓ cardiac output(hypotension-↓ pumping of LV),
soft&distant tones of the heart (apex beat,heart sounds), enlargement of the heart(pear shaped/globular)

EMERGENCY CARE
Tamponade: Puncture/pericardiocentesis,& conventional surgical approach

13. ANGINA PECTORIS

DEFINITION
AP is chest pain/ struggling sensation that is the product of transient myocardial ischemia . In 95 % of cases, is due
to focal narrowing of vv due to artherosclerotic . In 5% is exclusive cases , dif angina connected with other cause eg
hypercoagulation in oncological problem

PATHOGENESIS
Ischemia happens when there is demand and supply disbalance
1. When only demand is  ( dynamic changes )
 exacerbation
 rare because muscle are changed  supply change
 in special condition if accompanied by anemia
 below artherosclerotic plaque
2. Supply is impaired, demand not 
 eg when walking, x exhausted when at normal but when artheroma too big  slight movement and
psychological activation cause demand supply disbalance

3. Demand increase and supply decrease

 has artheroma  cause focal narrowing of vessel ( covers > 50 % ) patient can’t do activity  vv can’t
compensate the heart work

Problems in the vv that decrease supply

1. fixed occlusion of vv
2. Atheroma
 asymmetric part of atheroma n lumen can’t provide enough supply
 symmetric distribution – all parts of atheroma and can’t be compensated

3. Atheroma are normally stable – in some cases , nonspecific factors eg changes of vessel tone, spasm , poison,
 concentration of LDL  destabilize anatomy of atherosclerotic atheroma  breaks atheroma injury  content
of atheroma go to blood  coagulation activation ( adherence of platlet in 10-15 min )  thrombi to cover defect 
 lumen size so  blood flow
4. In stable condition , organism try to compensate. In localised narrowing  due to dilatation by regulating
factors. Exm of dilating factors are NO, adenosine and prostacycline

Main mechanism due to spasm of artery and transient hypercoagulation

 Spasm
1. central deposited spastic reaction provide through hyperactivity of  receptor localised in large and middle
sized coronary artery .
 overactivity of  receptor cause general spasm of coronary system
 spasm of these large trunk cause  in blood and o2 supply
2. Disbalance of and  receptor
  receptor dilate coronary system in stress condition
3. Atherosclerotic plaque  damage endothelium

 Hypercoagulation
- coagulation of artery depend on thrombocyte activation

CLASSIFICATION
I. STABLE
 aar of mainly fixed occlusion caused by atheroma ( not spasm )
 div to 4 grades acc to tolerance to physical activity ( Canadian Cardiology Society )
GRADE 1 Pain in physical activity in higher than normal activity due to  demand
GRADE 2 Common attacks of angina which is walking 100- 500m , climbing > 1 floor, walking
against frozen cold wind
Prominent angina when > 2 vessel affected , change in the lumen , stereotypic
GRADE 3 Pain at rest, at night  angina starts during REM sleep ( ↑ SNS  ↑ demand )
GRADE 4 Few patient survive till here , pain when walk < 100m , can’t carry up themselves , can’t
do anything simple, typical rest angina attack
Decubitus variant and nocturnal
20-50 attacks /day may occur

I. UNSTABLE ANGINA
 due to dynamic spasm
 div to 3 groups

a. Progressive exertional / accelerated angina

 patient > stable
 duration of attack/ year  15-20
 tolerance to physical activity very short
 NG not so effective

b. New onset angina

 suddenly appear
 can’t predict the outcome

c. Variant/ Prinzmetal angina

 appear only at rest and physical activity don’t provoke it
 it is pure spastic angina
 angina > prolonged
 > severe pain
 no absolute effect of NG

Post infarction angina

 at period of infarction within 1-8 weeks
 it is complication of infarction
CLINIC OF CORONARY PAIN SYNDROME

 Pain is reaction of organism when low blood supply ( energetic disbalance )

 In  no pain receptor , only supplied by specific receptor baroreceptor, chemoreceptor, mechanoreceptor
 In ischemic zone has overactivity of receptor   electrical function to brain  reach thalamus and irradiate
to cortex
 Character of pain is transient
 Localization : Pain localised in the chest , substernal area and may be on the left side @ others
 Duration : short  never exceed 20-30 min normally 5-10 min
 Physical activity like walking , climbing, carrying heavy things, psychostress cause  SNS
 Nitroglycerin sublingual relieve pain in < 5 min
 Irradiation : to central part of the chest , left shoulder, scapula region, jaw, arm, hand till 4th & 5th finger
 Character of pain : struggling sensation, heaviness, squeezing of the ♥ , burning, sharp pain, not stabbing and
localised pain which can be shown by finger
 Ass symptoms : headache, dizziness, inspiratory dyspnea, arrhythmic pulse, nausea
PHARMACOLOGICAL & STRESS TESTING: INDICATION, C/I & EVALUATION OF RESULT

Pharmacological test
 use Quarantide/ Dipyridamole 0.75ml/5min IV VD,or Isoprotenolol, or Albumetrin test
 inject IV to create organism for changes in blood flow for coronary system  find ST/T deviation
 eg Dipyridamole distribute blood flow  so provoke exacerbation of ischemia
Stress test
 also called provocating test
 don’t need to wait demand supply disbalance
 so common step test, ergometry ( walking, cycling ) when controlled, treadmill
 can give artificial condition to test the ♥ function before angina occurs
 Provocation  BP X HR at moment of investigation

Age Watt ( bpm )

20-30 170
30-40 150
40-50 150
50-60 140

 stress test for people > 60 yrs old not done

 physical work done step by step in 2 variants
a. non stop – increasing in mechanical load
b. 1 min of rest after each step for old people

 record ECG in next few minutes 2,3,4,5,10

 some people can reach submax level without changes in ECG
 inflammatory changes / dystrophy process in the heart check in ECG and clinical signs
 Clinical prove of angina :
a. if patient stop before or have sudden chest pain provoked by testing
b. changes in BP –if BP < 25-30% stop test and if BP > 220/110 stop the test

Group of ischemia contraindicated for stress test :

a. has fresh angina MI within 2 weeks of infarction
b. unstable angina
c. acute/ chronic respiratory failure ( 3rd grade )
d. Heart failure ( acute/ chronic )
e. Stenosis of the aortic valve because heart restriction to increase ejection
f. Arrhytmia
g. Tachycardia
h. Disease of joints and NS

RESULT : sensitivity of stress test ( 75 % ) , may be false @ patient don’t show problem in test / hyperdiagnostic

GENERAL MANAGEMENT OF ANGINA PECTORIS

Group of antianginal remedies :

A. Nitrates – sublingual @ IV
 don’t cure but only stop pain
 cause redistribution of blood because it is vasodilator
 3 forms of nitrates taken :
 immediate ( nitroglycerin ) – sublingual see effect in 2-3 min and max in 5-7 min ( t1/2 is 10-15 min )
 Dinitrate isosorbide – tablet with long term life in organism – per os
 NG in IV – indication for patient with acute coronary syndrome
A. β blockers
 Gen I – Propanolol  non selective β blocker with short term duration , 3-4 hours
 Gen II – selective group, Atenolol
 Gen III – Nebivalol
A. Ca channel blocker
- Verapamil, Diltiazem,

INDICATION OF SURGICAL TREATMENT

 3rd class angina pectoris

 stenosis of > 75% of 3 coronary vessel
 no effect of drug

PROGNOSIS

1st and 2nd grade angina pectoris have good prognosis but 3rd and 4th grade bad prognosis

UNSTABLE ANGINA PECTORIS ( PROGRESSIVE EXERTIONAL TYPE )

III)
PATHOGENESIS, CLINICAL PICTURE
 due to dynamic spasm
 div to 3 groups
a. Progressive exertional / accelerated angina
 patient > stable
 duration of attack/ year  15-20
 tolerance to physical activity very short
 NG not so effective

b. New onset angina

 suddenly appear
 can’t predict the outcome

c. Variant/ Prinzmetal angina

 appear only at rest and physical activity don’t provoke it
 it is pure spastic angina
 angina > prolonged
 > severe pain
 no absolute effect of NG
TACTIC OF MANAGEMENT
 hospitalization
 monitoring of BP
 stop pain, if oral NG not effective use opiode IV or NG IV under BP control
 β- blocker ( Metaprolol )  2x/day, IV
 heparin IV
 Metabolic therapy
 If stable condition , send to ward with aspirin substitute opiode , give β blocker , Metaprolol and tablets of NG
 Discharge after 10 days

STABLE ANGINA PECTORIS

CLASSIFICATION OF THE GRADES

GRADE 1 Pain in physical activity in higher than normal activity due to  demand
GRADE 2 Common attacks of angina which is walking 100- 500m , climbing > 1 floor, walking against frozen
cold wind
Prominent angina when > 2 vessel affected , change in the lumen , stereotypic
GRADE 3 Pain at rest, at night  angina starts during REM sleep ( ↑ SNS  ↑ demand )
GRADE 4 Few patient survive till here , pain when walk < 100m , can’t carry up themselves , can’t do
anything simple, typical rest angina attack
Decubitus variant and nocturnal
20-50 attacks /day may occur

CLINICAL SYMPTOMS
 main symptom is pain in constant situation
TREATMENT ACCORDING TO GRADES OF THE ANGINA
In 1st and 2nd grade angina :

1. NG in hand and patient should know the level of cholesterol if > 6.2 mmol/l. Use statins , fibrates , nicotinic
acid
2. Control hypercoagulation
3. Intake of β agents if have demand supply imbalance .Use statins to control A/S, can be substituted with nitrates
if have contraindication for β blocker. If nitrate is contraindicated use Ca channel blocker

In 3rd grade angina :

 β blocking agent + nitrate , Ca channel blocker + nitrate , β blocking agent + Ca channel blocker
 if not sufficient  do surgery ( bypass surgery by creating new shunt from proximal to distal part of the vessel )
 operation don’t treat fully coz new atheroma may appear
 So need to change lifestyle including smoking, diet,etc

In 4th grade angina :

 same like 3rd but success rate is low coz many plaque
 so only maintain the condition and surgery done
SPONTANEOUS ANGINA

PATHOGENESIS

CLINICAL PICTURE

INVESTIGATION

TREATMENT

DIFFERENTIAL DIAGNOSIS OF STABLE & UNSTABLE TYPES

14. MYOCARDIAL INFARCTION

EPIDEMIOLOGY. RISK FACTORS. PATHOGENESIS

- MI is the necrosis of the myofibril due to development of total occlusion of the coronary arteries caused by
thrombosis.

Epidemiology :
- This disease is widespread. In 1000 people, presence of 1-5 cases.
- So, there are more than a million cases in US, Russia.
- Mortality is more than 15% (primary infarction); if secondary (reoccur disease), its 30%.

Risk Factors :
- Age
- Sex
- Familial hypercholesterolaemia
- Smoking
- Stress
- Family history of MI
- Hypercoagulability of blood
- Hypodynamia
- High intake of fatty food

Pathogenesis :
- Pathogenesis of MI depends on the specific etiological factors.
- Self fixed occlusion by atheroma that grows along the years & causes occlusion of the coronary vessels.
- Spasm which can last more than ½ hour resulting in occlusion of the vessel too.
- Hypercogulation of the blood especially after the place of atheroma, blood moves slowly in vessels causing the
development of thrombosis of the vessel resulting in the occlusion.
- All these factors results in one common occlusion of the coronary artery. This causes no blood supply to the
myocardium resulting in the necrosis of the myocardium.

CLASSIFICATION
- Acc investigation of ECG, MI is divided into :
i.) ST-segment elevation MI.
ii.) Non-ST segment elevation MI.

- Acc etiology :
i.) MI caused by atherosclerosis ( 95% ).
ii.) MI caused by other reasons such as trauma, polycythemia, embolism, atheritis ( 5% ).

- Acc Clinical Pic if Infarction :

i.) Anginous form.
ii.) Asthmatic form
iii.) Abdominal form
iv.) Cerebral form
v.) Arrythmic form
vi.) Painless/Silent form

TYPICAL CLINICAL PICTURE

- Presence of ischemic coronary pain.
- Pain is crushing, oppressing, squeezing, heaviness & exarcebate in time. Its impossible to overcome pain. Next
day, pain disappears because of damage of all tissue that can die.
- It can become severe & patient can fall into shock.
- Pain is located in the sub sternal area.
- Pain prolonged more than ½ hour till next day.
- Irradiation to left shoulder, left arm & sometimes right shoulder.
- Affect of nitroglycerine is absent. Within ½ hour, patient cant move (to ↓ pain); sit flat calmly, but not so useful.
- They become restless.
- Next, is the secondary inactive period due to hypertensive crisis caused by infarction.
- Can have dyspeptic syndrome ( nausea & vomit ) due to vagus activation.
- If patient is at home, infarction cant provide to sleep.
- Patient can also have giddiness, anxiety & weakness together with the pain. Also presence of pale skin, cold sweat
& coldness in extremities due to ↓ arterial pressure.

CLINIC OF ATYPICAL VARIANTS

i.) Asthmatic Type :
- Pain is absent; attack of cardiac asthma.
- Dyspnoe with tachypnoe, cold sweat, palpitation, fear of death, weakness, orthopnoe & presence of rales.
- Typical for old ppl more than 65 years old (activation of sympatho-adrenalic ↓, PNS ↑). Old less intensive feel
pain, presence of metabolic change due to involution (↓ pumping activity).
- Also occurs in those who have MI in past. They obtain new changes for MI development.

ii.) Arrythmic Type :

- Combined without pain.
- Presence of pailpitation, dizziness, fast & irregular pulse.
- Often in patient more than 40 years old.
- Mainly ventricular arrhythmia, extrabeats, blocks, transient arrythmias.

iii.) Central/Brain Dependant Type :

- Looks like stroke; loss of consciousness.
- Impaired movement extremities one side; impaired feeling of skin, can speak; paresis of muscle.
- When infarction area is big, so, brain reacts to hypoxaemia (due to ↓ ejection of heart).
- When organism try to stimulate with compensatory activity, brain function improve & become conscious.

iv.) Silent Infarction :

- Pain absent; arrhythmia not present; no heart failure.
- Might have discomfort in chest, pain in the teeth or tip of finger.
- When necrosis not so huge; also for diabetic patient when got damage of pain receptors by polyneuropathia.
- If not treated, can be fatal sudden death.

INVESTIGATION
i,) Lab Test :
1 Enzymes – Episode of transient elevated enzyme level :
 1st is creatine phosphokinase (non specific). It has 2 isoenzymes (MB fraction that’s important in heart). This
enzyme after pain appear at the 1st 6 hours & peak for the next 24hours. Next day, enzyme is absent.
 2nd is AST, ALT. It increases gradually in 1st 6 hours & peak next day till 3rd-4th day; then disappears.
 3rd is LDH. Max 5th-7th day after onset of infarction & disappear after 2weeks.
- Troponins are elevated at end of 1st & 2nd day.
2 Leucocytosis Reactive – Max 1-2days; disappears at end of 1 st week. ESR ↑ in 1st week. Shift formula to the
left when bone marrow active regeneration. ↑ band leucocytes (in 1st 1-3days).
 In transmural infarction, got 1 specific sign : Aneosinophilia in 1st/2nd after infarction; then it reappears again.
Might ↑ quantity of myoglobin in blood. Can have transient hyperglycaemia (less tha 8m.mole/l); dony appear
in urine. In hyperglycaemia more than 8m.mole/l, patient has DM.

ii.) ECG (Transmural Type) :

1 Normal R-wave in affected area accompanied with horizontal ↑ of ST : Shows transmural ischemia.

2 If more than ½ hour, its acute stage. Necrosis spread to all layers (6hours-5 or 7 days). Main wave show
electrical activity. R-wave disappear. Still got elevation of ST; Pic of ECG is QS complex.

10 Elevated T-wave; there is other variant of this same stage.

1 When myocardium start to recover & scar begin to form is Subacute ohase. Person still has QS-wave. Pic
of QS syndrome look like still elevated ST; amplitude greatly decreased.

2 Picture of scarring :

* In posterior infarction, dissapearence of R-wave not typical; but Q-wave is still present.

* There are 2 rules. If Q-wave appear by amplitude more than ¼ R-wave, its pathological. Or if its wider tha 0.03s :

Non Transmural Type :

- Subendocardial & intramural.
- It can stay 2 days after onset of infarction.
- Change in ST & T-wave only; Q-wave don’t exist.
- After 8 weeks, there is no trace of any changes.

iii.) Ultrasound :
- Shows discoordination activity of myofibrils.
- Sectoral investigation of heart contractility – Heart divided into different zones acc areas supplied can confirm MI
in these zones.
- Can find only localized disorder of myocardium; whether its old/fresh MI, its difficult to say.
- We can look aneurysm of heart, dyskinesis or akinesis of myofibrils.

iv.) Imaging methods :

- Presence of many changes in MI.
- Can use Talium/Tecnesium method – Absence or more high concentration of radioisotopes.

DIFFERENTIAL DIAGNOSIS OF UNSTABLE ANGINA

MAIN PRINCIPLES OF TACTIC

- Firstly, treatment should be given to patient to treat or reduce the chest pain. For this, patient given :
i.) Nitrates should be given 1 st sublingually or by buccal spay (0.3-0.6mg). If pain persists after 3doses given
5minutes apart, IV nitroglycerine (5-10microgram/min) given. The rate of infusion can be increased to
10microgram/min every 3-5minit until symptoms are relieved.
ii.) Beta adregernic blockers : IV beta blockers (Metoprolol/Esmolol) followed by oral beta blockers targeted to
heart rate of 50-60beats/min.
iii.) If pain still persist, morphine sulfate 1-5mg IV can be given every 5-30minutes.

- Next, thrombolytic treatment should be given. This is done by giving drugs such as :
i.) Streptokinase (1.5 million units/hour).
ii.) Urokinase
iii.) Tissue type plasminogen activator (t-PA)

- This treatment is followed by anticoagulating treatment. Anticoagulants should be given to patient :

i.) Heparin (unfractioned heparin) – Bolus 60-70 U/kg (max 5000 U) IV followed by infusion of 12-15 U/kg/hour.
ii.) Enoxaparin (Lovenox) – 1mg/kg subcutaneous every 12hr.
iii.) Dalteparin (Fragmin) – 120 IU/kg subcutaneous every 12hr (max 10000 IU twice daily).
11 When the ECG reading of the patient normalizes, aspirin 75-150mg daily is given to patient unless
contraindicated.
12 These could be combined together with beta-blockers & ACEinhibitors.

TREATMENT OF PAIN SYNDROME (TACHI- & BRADIARRHYTHMIAS)

- To treat pain :
i.) Nitrates should be given 1 st sublingually or by buccal spay (0.3-0.6mg). If pain persists after 3doses given
5minutes apart, IV nitroglycerine (5-10microgram/min) given. The rate of infusion can be increased to
10microgram/min every 3-5minit until symptoms are relieved.
ii.) Beta adregernic blockers : IV beta blockers (Metoprolol/Esmolol) followed by oral beta blockers targeted to
heart rate of 50-60beats/min.
iii.) If pain still persist, morphine sulfate 1-5mg IV can be given every 5-30minutes.

- To treat arrhythmia :
i.) Quinidine (class IA) – Oral 200-400mg q6hour
ii.) Lidocaine (class IB) – IV 20-50mg/min
iii.) Sotalol Orally 80-320mg q12hr

ANTICOAGULANT & FIBRINOLYTIC THERAPY

- Drugs used in Fibrinolytic therapy are :
i.) Streptokinase (1.5million units/hour)
ii.) Urokinase
iii.) Tissue type plasminogen activator (t-PA)
- Anticoagulant used are such as :
i.) Heparin (unfractioned heparin) – Bolus 60-70 U/kg (max 5000 U) IV followed by infusion of 12-15 U/kg/hour.
ii.) Enoxaparin (Lovenox) – 1mg/kg subcutaneous every 12hr.
iii.) Dalteparin (Fragmin) – 120 IU/kg subcutaneous every 12hr (max 10000 IU twice daily).
COMPLICATIONS OF EARLY PERIOD. CAUSES

CLINICAL SYMPTOMS & DIAGNOSIS

CARDIOGENIC SHOCK. TYPES. PATHOGENESIS. CRITERIA

- Cardiogenic shock is the crisis if microcirculation & its due to the spread of infarction (in main trunk of left
coronary artery).
- There are 4 types :
i.) True cardiogenic shock (damage more than 40% myocardium). Mortality 95%.
ii.) Reflex cardiogenic shock (not connected with severity of infarction). Depend of receptor sensitivity in brain &
opioid system. If work badly, shock develops.
iii.) In permanent ventricular/fibrillation – Develop shock due to disorganization pumping.
iv.) Areactive shock – When dopamine, epinephrine not effective when receptor of patient blocked for alcoholic,
drug addicts/ because receptor is well adapted to epinephrine.

Pathogenesis :
- Decreased ejection in shock due to blocking contractility of myocardium in MI/Rx drop in inotropic function by
brain in pain (spasm of peripheral vessels).
- Flow of blood decrease in brain, kidney.
- Arterial system empty, blood move slow, stagnate in peripheral area, decreased preload, liquid blood come out to
the interstitial system.
- After 6-12hrs, organ start to die – Reduced liver activity,etc.
- After 12hrs, it changes to irreversible organ type of shock.

Criteria of shock : Patient look pale, cold, got diffused acro-cyanosis (bluish element due to dilatation of capillary
loop; Marble skin.
- They lie flatly, condition is spoor/stupor; rarely talk. Also there is decreased cortex blood, reduced urine less than
20ml/hour. In 24hours, lesser tha ½ - Acute renal failure.
- Systolic BP less than 60; diastolic less than 40; pulse pressure less tha 20.
- Can have dev of psychosis (decreased AP less than 80).

EMERGENCY CARE. REHABILITATION. SECONDARY PROPHYLAXIS. PROGNOSIS

15. ESSENTIAL HYPERTENSION & SECONDARY HYPERTENSION

ESSENTIAL HYPERTENSION
DEFINITION
1 Def: it’s the condition in which elevated art P is the leading symptom(sys: >140, diastolic> 90). Disease is
provoked by nervous & functional disorders in reg of vascular tone.
EPIDEMIOLOGY
2 > 50% of ppl have this disease
3 prevalence in man
4 15-37% of global population got HPT
5 Average BP in Europe – 136/83 (age: 35-74)
6 Highest in Germany

ETIOLOGY
1 Genetic- 2x risk if 1 or both parents have
2 Diet- high salt, alcohol (alcohol inhibit barorcptor, so x control BP. It also ↑es Angiotensin I productn
causing abnormality in Na-K pump.
3 Obesity
4 Racial: African American
5 Personality: Hostile, time urgent
6 Stress : cause disbalance in SNS & PNS in catecholamine release.

PATHOGENESIS
1 2 theories of dev:
o Neurogenic/Neurologic- due to dysfunction of cortex & subcortical struc with activated vasopressor
mchnsm (older theory)
o Mbrane transport prob thru cell mbrane- Na & K transport disturbances→ contractility & sensitivity of
vessel mm ↑ (vasospasm)
2 Mechanisms:
o Pressor:
1) SNS – tachycardia, spasm of perivessels
2) Ag-renin system- ACE &Ag II – (very active vasospastic enzyme)
3) Aldosterone- reabsorptn of Na, ↑ blood circ.
1 Counter:
1. Kalikrein kinin system
2. Prostaglandin
3. Prostacyclin E
4. Baroreflex system (at carotid sinus, aortic arch)

CLASSIFICATION
1 Acc to degree:
o Mild (I) : 140-159(s) 90-99 (d)
o Mod (II) : 160-170 100-109
o Severe (III) : >180 >110
o Isolated sys : >140 <90

2 American classification:
o Normal: <120 <80
o Pre- HPT: 120-139 80-89
o Stage I HPT: 140-159 90-99
o Stage II HPT: >160 >100

CLINICAL PICTURE ACCORDING TO STAGES

1 Stage 1 : no changes in organ target
2 Stage 2: got changes in organ target (Hypertrophy of LV, changes in heart, microalbunemia fr kidney,
hypertrophy- angiopathy from brain)
3 Stage 3: Complication from organ target
o Brain: encephalopathy insult
o Heart: Ischemic heart disease, M.I
o Kidney: kidney insufficiency
Symptoms:
1 Increase BP
2 Headache (in occiput or diffuse) + vertigo
2 Pain in the heart -(cardialgia bcoz of ↑ Art P- local intensive pain in apex region)
- hemodynamic Angina pectoris (strangling pain) bcoz b/flow not
adequate to hypertrophied mm- (dev ischemic pro)
1 Tachycardia
2 Extra beat
3 Flushed face
4 Fatigue ,nervousness
5 Vomiting , nausea maybe present

INVESTIGATION
1 Obj : measure Art P in all extremities. (both hand absolutely)
2 Percussion of heart: enlargement of Left heart borders
3 Aus: systolic murmur at apex, accentuation of S2 above aorta
4 Blood analysis : K, Ca, Na,
5 Sugar rXn : for glu level
6 Urine analysis: check level of creatine.
7 microrXn
8 ECG: LV hypertrophy
9 Xray- LV hypertrophy, heart enlargement
10 Echocardiography
11 Us of heart
12 Specific tests:
o Brain- rheography ( to see cerebral vessels), encephalography,
o Kidney- Zimnitsky test,Nichiparenko, US, contrast angiography , contrast urography, biopsy
o Eyes-check aa (for retinopathy, papiloedema, etc)
o Consult neuropathologist, occulist
o Hormone levels – thyroid, glucocoticoids, cathecolamines

COMPLICATIONS
1 CNS:
o Stroke : cerebral HR or infarction
o Hypertensive encephalopathy : transient disturbance of speech, disorientation, fits, unconsciousness
o Subarachnoid HR
2 Retina:
o Grade 1: Mild arteriolar narrowing
o Grade 2: >marked narrowing + appearance of arterio-venous nipping produced when thickened retinal
aa pass over retina
o Grade 3: grade 2 + flame-shaped HR & soft cotton wool exudates
o Grade 4: G3 + papiloedema
3 Heart:
o LV hypertrophy→ failure
o IHD, heart failure
4 Kidney
o Proteinuria
o Progressive renal failure

PROPHYLAXIS OF COMPLICATIONS
1 Adequate Tx of pharmalogical & non pharmalogical alternatives to maintain the level of arterial Pressure.

TREATMENT ACCORDING TO STAGES & PATHOGENETIC

Non pharmaco: improve diet, x physical exertion (strenuous sports), only dynamic (walking, running, swimming),
stop smoking
1 Pharmaco (depend on stages)
 1. Hyporenin form- give diuretics: thiazides
2. Hypokinetic type (tachycardia, high syst P)- give B blockers
3. renal (activated rennin-Ag activity) – ACE inhibitor : lozartan
4. high diastolic- vasodilators :nifidepine

1 Scheme of treatment
1) BB @ D
2) BB +D
3) BB + D + Vdilators
4) BB + D + ACEIs + VDtors
5) Vdtors + central mchnsm of activity

2 Tailored antihypertensive therapy

1) CHF : D+BB+ ACEI + ALD
2) Post MI : BB + ACEI + ALD + ANT
3) CHD HIGH Risk :D + BB +ACEI + CCB
4) DM : D + BB + ACEI + ARB
5) Chr Kidney : ACEI + ARB
6) Stroke prevention : D+ ACEI

PROGNOSIS
3 If treatment is adequate- prognosis is good
4 If development of crisis & there is no treatment- prognosis is bad

SECONDARY HYPERTENSION
DEFINITION
arterial P rises as a symptom of some other disease. ( x the leading symptom).

ETIOLOGICAL GROUP OF CAUSES

1) Central/ cerebral form
5 main cause : trauma, infection : meningitis, arachnoiditis, encephalitis

2) Hemodynamics art HPT

6 coarctation of aorta – congenital, charac: ↑bp in arms,↓ in legs
7 aortic insufficiency
8 artherosclerosis of aorta

3) Drug art HPT

1 caffeine containing drugs
2 ephedrine containing drugs
3 narcotics

4) Endocrine HPT
1 hyperthyroidism –( tachycardia, high level of thyroid P, high syst P)
2 hypothyroidism – high diastolic P aar of edema of walls of vessels
3 Acromegaly- hypophysis disorder
4 Cushing’s disease/ syndrome – suprarenal tumors (charac: obesity, fat localized only on body, osteoporosis dev,
DM, hypertrichosis developmt, probs with sexual funct dev & ↑ art P)
5 Conn’s syndrome – weakness of m constructn, alkaline rXn of urine, low K level
6 Pheochromocytoma

5) Renal HPT
1 Parenchymal : GN, PyN, polycystosis, hydronephrosis, TB, tumors, rheum disorders: nodulus periarteritis.
2 Renovascular : fistules, muscular dysplasia, tumor near vessels, artery diseases: aorta arteritis.

PROPERTIES OF CLINIC
1 Very high art P
2 No complaints- no headache, no pain in the heart
3 No effect of antihypertensive Tx . ( need to treat primary disease, then bp drops)
4 Has features of kidney disease : eg- face edema
5 If there is renovascular prob : surgical approach

INVESTIGATION
1 Same as primary hypertension

DIFFERENTIAL DIAGNOSIS FROM ESSENTIAL TYPE

Primary Secondary
No causes has a cause
In anamnesis : got ↑ BP In anamnesis : x ↑ BP
↑ level of both sys & diast bp Only ↑ of systolic normally
- Feature of coarctation of heart, valve disorders,
- Kidney disorders- face edema, urine changes
- CNS- trauma, brain inflammation

16. CARDIOMYOPATHY

CLASSIFICATION
 Obstructive hypertrophic (HCM)- char by variable myocardial hypetrophy, most commonly involving IV
septum, and disorganization of cardiac myocytes and myofibrils
 Dilatative (DCM) -char by dilatation and impared systolic function of the left ventricle and/or right ventricle, in
the absence of abnormal loading conditions eg HT, valve diseases
 Restrictive (RCM)-impaired ventricular filling

PATHOGENESIS
DCM: idiopathic cause, but in general involves deficiency of a certain gene encoding cytoskeletal or associated
myocyte proteins
HCM: familial autosomal dominant cause, involving mutations of gene encoding sarcomeric proteins
RCM: ?

CLINICAL SYMPTOMS
DCM: similar with those of left and/or right heart failure
 Dyspnea during slight physical extertion/rest
 Suffocation and cardiac pain inresponstive to NGlycerin
 Borders of heart displaced to right, upwards and left
 Heart sounds at apex dulled, 2nd sound over pulmo trunk is accentuated, gallop rhythm dev along with systolic
murmur
 Pulse is small and fast
 AP decreased (usually)

HCM:
1 Chest pain
2 Dyspnea
3 Syncope or presyncope
4 Cardiac arrhythmias
5 Sudden death
6 Atrial fibrillation
7 Double apical pulsation (forceful atrial contraction producing 4th heart sound)
8 Jerky carotid pulse
9 Ejection systolic murmur
10 Pansystolic murmur dt mitral regurgitation

RCM:
1 Dyspnea
2 Fatigue
3 Restriction to vent filling (persistently elevated venous pressure)
4 Ascites and dependant edema
5 Friedreich’s sign (high jugular venous pressure with diastolic collapse)
6 Kussmaul’s sign (elevation of venous pressure with inspiration)

INVESTIGATION
DCM:
 Chest x-ray demonstrates generalized cardiac enlargement
 ECG shows diffuse non-specific ST segment and T wave changes
 Echocardiogram reveals dilatation of left and/or right ventricle with poor contration function
 Angiography

HCM:
1 Chest x-ray usually unremarkable
2 ECG demonstrates left vent hypertrophy and T wave changes, abnormal Q waves
3 Echocardiogram shows asymmetric left vent hypertrophy
4 Pedigree analysis reveals autosomal dominant inheritance
5 Exercise test and ECG ambulatory recording

RCM:
1 Chest x-ray show pulmo venous congestion
2 ECG has low-voltage and ST segment and T wave abnormalities
3 Echocardiogram show symmetrical myocardial thickening and impaired ventricular filling
4 Cardiac cathetherization helps distinct from constrictive pericarditis
5 Endomyocardial biopsy

TREATMENT
DCM: goal is to relieve symptoms, retard disease progression and prevent complications.
 Diuretics
 ACEI’s
 Beta blockers
 Implanted defibrillators
 Still in studies: GH, immunoadsorption, anti-cytokine therapy

HCM: goal is to prevent sudden death

1 Beta blockers, verapamil (to treat chest pain)
2 Disopyramide
3 Resection of septal myocardium
4 AVOID vasodilators

RCM: no specific treatment

1 Melphalan plus prednisalone to treat primary amyloidosis
2 Colchicines
3 Transplantation

COMPLICATIONS
PROGNOSIS

17. DISEASESES OF PERICARDIUM. DRY, EFFUSION & CONSTRICTIVE PERICARDITIS

PATHOGENESIS
-in most cases pericarditis dev in the presence of rheumatism or tuberculosis
-rheumatic pericarditis usually concurs with affection of the myocard and endocard
-rheumatic, and mostly tuberculous pericard are manifestations of infectious allergic process.
-in certain cases, tuberculous pericard depends on the spread of infection from the foci in the lungs and
tracheobronchial lymph nodes (via the lymph ducts to the pericardium).
-pericarditis can dev in other infections as well (eg scarlet fever, measles, influenza, or sepsis)
-sometimes it dev due to transition of inflammation from the adjacent organs in pleurisy, pneumonia, MI, and also in
injuries to the heart and uraemia.

CLINICAL PICTURE
Dry pericarditis:
 Chest pain that is substernal and sharp (relieved by sitting forward, may referred to neck or shoulders)
 Pericardial friction rub (cardinal sign), heard best at lower left sternum, leathery triphasic sound

Pericardial effusion:
1 Pressing sensation in chest and pain in heart
2 Dyspnea and dysphagia
3 Fever is common
4 Appearance is edematous, skin is cyanotic and pallied
5 Neck veins are swollen
6 Orthopnea position
7 Apex beat obsured by effusion, soft heart sounds
8 Enlargement of cardiac dullness in all directions
9 VP elevated

Constrictive pericarditis:
1 Systemic venous congestion – ascites, dependant edema, hepatomegaly and jugular venous distension
2 Signs of impaired ventricular filling (Kussmaul’s sign)
3 Friedreich’s sign
4 Pulsus paradoxus
5 Fatigue and exercise intolerance
6 Atrial fibrillation and loud 3rd sound revealed

INVESTIGATION
Dry pericarditis:
1 ECG is diagnostic-During 1st few weeks, ST elevation in ant, lat, inf leads. Only AVR, V1 show ST depression.
Later ST segment normalize and T wave inversion present. Present also sinus tachycardia
2 Blood analysis: Leucocytosis -> lymphocytosis, increase of cardiac enzymes

Pericardial effusion:
1 ECG shows low voltages
2 Chest x ray demonstrate large globular or pear shaped heart with sharp outlines
3 EchoCG most useful for demonstrating effusion and right ventricular collapse during late diastole
4 Doppler may show increased flow through tricuspid and pulmo valves
5 MRI – detect hemopericardium

Constrictive pericarditis:
1 Chest x-ray: shows relatively small heart with obvious calcification seen on lateral film or by using fluoroscopy
2 ECG: may show low QRS voltage and T wave inversion
3 EchoCG: may demo thickened pericardium with calcification over right heart and relative immobility
4 Cardiac catheterization and MRI: typically, diastolic pressure equal in all 4 chamber.

TREATMENT
Dry pericarditis:
1 Anti-inflammatory drugs (aspirin at high doses 600-900 mg every 6 hours)
2 Indometacin 25-100mg every 4 hours, ibuprofen 400mg every 6 hours for symptom relief.
3 Systemic corticosteroids eg prednisalone 20-80 mg daily
4 Azathioprine 50-100mg daily, colchicines 1-2 mg/dL in cases of corticort-resistance

Pericardial effusion:
1 Pericardiocentesis
2 In cases of reaccumulation, pericardial fenestration either transcutly via balloon pericardiotomy under local
anesthesia or by using conventional surgical approach
3 ?

Constrictive pericarditis:
1 Surgical removal of substantial portion of the thickened pericardium provides a cure
2 In others, persistent constriction, atrial fibrillation and myocardial fibrosis prevent full recovery