عسى الله أن ينفع بها ---

1. Cases in cardiology
DR.MAGDI AWAD SASI
CCU
7TH
OCTOPER HOSPITAL
BENGHAZI
LMB—BENGHAZI UNIVERSITY

2. A 55-year-old man with a history of diabetes,
hypertension, hyperlipidemia, and current smoking
presents with a 2-month history of progressively
worsening chest pain on exertion. Which of the
following diagnostic procedures is most appropriate
A. Exercise ECG testing
B. Adenosine myocardial perfusion scintigraphy
C. Dobutamine stress echocardiogram
D. PET scan
E. Cardiac catheterization

3.  E

4. A 35 year old woman with a history of rheumatic fever in
childhood had had episodes of congestive heart
failure for several years. During the last of her
hospital admissions, she developed massive
pulmonary thrombo-embolism and died. Autopsy
examination showed that her lungs were firm and
brown, and microscopically had widened, edematous
and fibrosed alveolar septa, aggregates of heart
failure cells in the alveoli, thickened small muscular
arteries, and atherosclerosis in the larger pulmonary
arteries. An acquired valvular disease was found in
the heart. Which one of the following was it most
likely to be
A. MITRAL STENOSIS.
B. TRICUSPID STENOSIS.
C. AORTIC STENOSIS.
D. AORTIC REGURGITATION.
E. MITRAL REGURGITATION

5. The Correct answer is A
rheumatic heart disease (isolated mitral stenosis in
25% of all cases of rheumatic h.d., mixed mitral
stenosis and regurgitation in 40 % of all cases of
rheumatic h.d.,( two third of patients – women(
IN ABOUT 50% OF PATIENTS WITH MITRAL STENOSIS
THE RHEUMATIC FEVER MAY BE UNRECOGNISED
VIRAL CARDITIS - VERY RARE CAUSE OF MITRAL
STENOSIS
TWO THIRDS OF CASES OCCUR IN WOMEN

6. Pathophysiology
-the mitral valve orifice
-NORMALLY ABOUT 5 CM2 (IN DIASTOLE)
- MODERATE STENOSIS (APPROX 2CM2) - PATIENTS REMAIN
ASYMPTOMATIC
- 1CM OR LESS IN SEVERE MITRAL STENOSIS
-in mitral stenosis cardiac output may be maintained by rise pressure in LA,
pulmonary venous and capillaries - it results in the loss of lung
compliance and the development of exertional dyspnoea
-MILD STENOSIS - ATRIAL PRESSURE RISES ONLY ON EXERCISE
-SEVERE STENOSIS - RAISED ATRIAL PRESSURE IS REQIURED TO
MAINTAIN CO EVEN AT REST
-THE RAISED ATRIAL PRESSURE - ENLARGED DIAMETERS OF LA (LA
DILATATION IN 80% OS CASES) - ATRIAL FIBRILLATION (SOMETIMES
THE FIRST SIGN OF CLINICAL DETERIORATION) - LOSS OF ATRIAL
CONTRACTION CONTRICUTE TO DIMINISHED VENTRICULAR FILLING
- RISK OF ATRIAL THROMBOSIS AND SYSTEMIC THROMBOEMBOLISM
)PARTICULARY THOSE WITH AF(
-SUDDEN ONSET OF ATRIAL FIBRILLATION - SUDDEN INCREASE IN
PULMONARY VENOUS PRESSURE - SOMETIMES PULMONARY OEDEMA
- THE LONG-TERMED MITRAL STENOSIS AND MORE GRADUAL RISE IN
PRESSURE - THE INCREASED PULMONARY VASCULAR RESISTANCE,
WHICH PROTECTS AGAINST PULMONARY OEDEMA
- RIGHT VENTRICULAR HYPERTROPHY AND PULMONARY HYPERTENSION
(RESULTS FROM : PASSIVE BACK-PRESSURE, ARTERIORAL
CONSTRICTION, OBLITERATIVE CHANGES IN PULMONARY VESSELS

7. SYMPTOMS
)most common in the third or fourth decade of life(
EXERTIONAL DYSPNOEA, NOCTURNAL DYSPNOEA,
COUGH, HEMOPTYSIS
LEG, ANKLE OEDEMA, ABDOMINAL SWELLING (RIGHT
VENTRICULAR FAILURE(
SYMPTOMS OF ACUTE PULMONARY EDEMA (AF,
PREGNANCY(
SYMPTOMS SECONDARY TO ARTERIAL (RARE VENOUS)
EMBOLI
SYMPTOMS OF DIMINISHED CO (FATIGUE, TIREDNESS(
Asymptomatic mitral stenosis - the physical signs of
mitral stenosis are found before symptoms develop

8. SIGNS
ATRIAL FIBRILLATION
MITRAL FACIES
AUSCULTATION
LOUD FIRST HEARD SOUND (THE STENOTIC VALVE PROLONGS ATRIAL
EMPTYING, LEAFLETS REMAIN OPEN AT THE ONSET OF DIASTOLE AND
ARE CLOSED SUDDENLY(
OPENING SNAP (THE OPENING SNAP GETS CLOSER TO THE SECOND
SOUND AS THE STENOSIS BECOMES MORE SEVERE, MAY BE
INAUDIBLE IF THE VALVE IS HEAVILY CALCIFIED(
MID-DIASTOLIC MURMUR (THE TURBULENT FLOW CAUSES THE LOW
PITCHED DIASTOLIC MURMUR, AND OFTEN A THRILL; MURMUR IS
ACCENTUATED BY EXERCISE AND DURING ATRIAL SYSTOLE-
PRESYSTOLIC ACCENTUATION; IT IS HEARD BEST AT THE CARDIAC
APEX WITH THE PATIENTS IN THE LEFT LATERAL DECUBITUS
POSITION(
SIGNS OF RAISED PULMONARY CAPILLARY PRESSURE
(CREPITATIONS, PULMONARY EDEMA, EFFUSIONS(
SIGNS OF PULMONARY HYPERTENSION (ABNORMAL PULSATION FELT
TO THE LEFT OF THE STERNUM, DUE TO EITHER TO RIGHT
VENTRICULAR HYPERTROPHY OR TO FORWARD DISPLACEMENT OF
THE HEART BY DILATED LA; LOUD THE PULMONARY COMPONENT OF
THE SECOND HEART SOUND; TRICUSPID REGURGITATION
SECONDARY TO RIGHT VENTRICULAR DILATATION CAUSES THE
(SYSTOLIC MURMUR AND SYSTOLIC WAVES IN THE VENOUS PULSE(

9. INVESTIGATIONS
INVESTIGATIONS
THE ECG :
THE LEFT ATRIAL HYPERTROPHY - P MITRALE (THE BIFID P WAVES)
OR ATRIAL FIBRILLATION
RIGHT VENTRICULAR HYPERTROPHY (THE EARLIEST SIGN -
REDUCTION IN THE SIZE OF THE USUAL QS COMPLEX IN THE
LEAD V1(
CXR
ENLARGED LEFT ATRIUM
SIGNS OF PULMONARY VENOUS HYPERTENSION (ENLARGEMENT OF
THE UPPER PULMONARY VEINS, HORIZONTAL LINEAR SHADOWS
IN THE COSTOPHRENIC ANGLES(
ECHOCARDIOGRAPHY: THICKENED IMMOBILE CUSPS, ENLARGED
SIZE OF THE LEFT ATRIUM, REDUCED VALVE AREA, REDUCED
RATE OF DIASTOLIC FILLING
CARDIAC CATHETERISATION: PRESSURE GRADIENT BETWEEN LA
AND LV

10. A 45 year old man presented with gradually increasing
shortness of breath and episodes of paroxysmal nocturnal
dyspnea. His blood pressure was 140/40 mm of Hg, the
pulse was bounding, and a blowing diastolic murmur was
heard in the right upper parasternal region. Chest X-ray
showed marked widening of the mediastinum due to
dilatation of the ascending aorta. The most likely
diagnosis is
a. Pneumococcal endocarditis of the aorta valve.
b. Atherosclerotic aneurysm of the ascending aorta.
c. Syphiltic aortitis.
d. Mitral stenosis.
e. Calcific aortic stenosis

11. The correct answer is C
Pathological consequences of syphilitic aortitis
The aortitis is mostly inflammation in the media and adventitia,
induced scarring causes an intimal wrinkling in the aortic
wall
Tree bark appearance, which is chx of syphillis
Inflammation and fibrosis in the aorta, just above the aortic
valve cusp is very problematic
Can narrow the coronary arteries, producing severe ischemia
Aortic valve dilates à commisures separate from each other à
when the valves close, there are gaps at the periphery à
aortic regurgitation, which can be severe
Many cases die from this, rather than from the ruptured
aneurysm

12. 65year old man had transfemoral catheterization for coronary
angiography which revealed the presence of severe
atherosclerotic narrowing of all major coronary arteries.
Within hours of the procedure, he developed severe left lower
quadrant abdominal pain. which was later associated with
rebound tenderness, livido reticularis (erythematous skin rash)
of the abdominal skin, increasing hypertension, cold blue toes
and progressively worsening renal failure.
Laparotomy revealed necrosis of the descending colon. This was
resected. Microscopic examination showed amorphous
eosinophilic material containing slit-like spaces occluding
arteries in the submucosa. Which one
of the following is the most likely explanation?
A. Thromboemboli secondary to myocardial infarction
B. Type B dissection of the aorta
C. Hypersensitivity vasculitis
D. Atheroembolism
E. Polyarteritis nodosa

13. The correct answer is D
Discussion
Atheroembolic disease increasingly is being recognized as an
important cause of morbidity and mortality in the developed world.
The true incidence of atheroembolism is not known, but it is likely
that many if not all adults older than 70 years will have evidence of
atheroembolism if it is sufficiently sought.
Even when the disease presents with the classic signs of digital
ischemia, livedo reticularis, and eosinophilia, other causes often are
sought. More often, patients present with a myriad of symptoms
because of cholesterol crystal deposition in small- and medium-
sized vessels. The clinical consequences range from pancreatitis to
penile gangrene. It is therefore not surprising that atheroembolism
has been described as a great mimicker. To make matters worse,
even when a diagnosis has been accurately established no
treatment has been shown to have a significant impact on the
attritional morbidity and mortality associated with atheroembolism
The clinical features of atheroembolism range from subclinical
disease to multisystem involvement leading to multiorgan failure
with an associated high mortality . The disease typically affects
white men 60 years of age and older. Established precipitants of
catastrophic atheroembolism are
o Preceding history of angiography or any instrumentation to the
aorta.
o Anticoagulant therapy.
o Cardiovascular surgery.
o Diabetes, hypertension, and previous vascular disease.
o Thrombolytic therapy (controversial (

14. A 57 year old man presents with a 35 minute history of severe chest
pain radiating down his left arm, associated with shortness of
breath. He denies denies a prior history of chest pain. His serum
troponin levels and EKG are compatible with an acute anterior
wall myocardial infarction. The histological finding you would
expect in the left anterior descending artery (LAD(
A. Circumferential medial fibrosis
B. Circumferential intimal fibrosis
C. Eccentric intact atherosclerotic plaques
D. Disrupted atherosclerotic plaque with non occlusive mural
thrombosis
E. Disrupted atherosclerotic plaque with occlusive thrombosis

15. Answer
E. Disrupted atherosclerotic plaque
with occlusive thrombosis
The rapid closure of coronary arteries
caused by occlusive thrombi is the major
cause of acute myocardial infarction.
Disruption of coronary atherosclerotic
plaques is recognized as one trigger of
coronary thrombosis. Formation of
thrombosis or hematoma may cause angina
pectoris or an acute coronary syndrome
due to occlusive thrombosis

16.  A 57 year old man presents with a 35 minute history of severe
chest pain radiating down his left arm, associated with
shortness of breath. He denies a prior history of chest pain. His
serum troponin levels and EKG are compatible with an acute
anterior wall myocardial infarction. The patient actually did
well initially, but collapsed outside his hospital room suddenly
6 days later. A new loud murmur indicating mitral insufficiency
was heard, but he died within 10 minutes. Of the following,
which is the most likely cause of death based on this history
A. Pulmonary embolism originating in left ventricular mural
thrombus
B. Ruptured ventricular papillary muscle
C. ruptured left ventricular papillary muscle
D. Acute bacterial endocarditis of mitral valve
E. Mitral valve prolapse

17. Answer
 C. ruptured left ventricular
papillary muscle
Ruptures can lead to papillary muscle
damage with acute mitral
insufficiency, which can lead to acute
hemodynamic changes on the left
side.

18.  The most common cause of death of in-
hospital patients with myocardial
infarctions
A. Cardiogenic shock (severe pump failure(
B. Arrhyrhmia
C. Cardiac free wall rupture
D. Rupture ventricular aneurysm
E. Constrictive pericarditis

19. Answer
B. Arrhyrhmia
 Ventricular fibrillation is the most common form of
arrhythmic death in acute myocardial infarction. The vast
majority of deaths due to ventricular fibrillation occur within
the first 24 h of the onset of symptoms, and of these
deaths, over half occur in the first hour.
 Most out-of-hospital deaths from myocardial infarction are
due to ventricular fibrillation. It may occur without warning
symptoms or arrhythmias.
 Over the last 30 years, with careful monitoring and prompt
attention to arrhythmias, the in-hospital mortality for acute
myocardial infarction has been reduced from about 30 to
between 10 and 15 percent.

20.  A 74 year old man presents with severe chest pain to the
emergency room, and is found to have a widened mediastinum
on chest radiograph and a murmur of aortic insufficiency on
examination. He dies on the operating table from blood loss
from a ruptured but very dilated ascending aorta. At autopsy,
severe aortic atherosclerosis, especially in the ascending
aorta, is seen together with a longitudinal intimal ridging
resembling tree bark affecting the ascending aorta. the aortic
root is also dilated. Histological sections of the aortic arch
confirm the atherosclerotic plaques, and also show
obliterative endarteritis of the vasa vasorum.
Your diagnosis:
A. Kawasaki arteritis; atherosclerosis
B. Atherosclerosis with secondary bacterial aortitis
C. Aortic dissection., Type A
D. Syphilitic aortitis with accelerated atherosclerosis
E. Takayasu arteritis

21.  D. Syphilitic aortitis with accelerated
atherosclerosis
Syphilitic aortitis causes obliterative
endarteritis of the vasa vasorum. This leads
to ischemia and smooth muscle atrophy of
the aortic media& can cause dilation of the
aortic ring leading to aortic insufficiency.

22.  A 93 year old man has a syncopal episode after being well most
of his life. Workup reveals aortic stenosis and you plan to
operate. You expect to find:
A. A calcified triscupid aortic valve without fused commisures; a
normal mitral valve for age

B. A calcified tricuspid aortic valve without fused commisures; a
normal mitral valve with fused, thickened chordae

C. A calcified tricuspid aortic valve with fused commisures; a
normal mitral valve for age

D. A calcified bicuspid aortic valve; a normal mitral valve for age

E. A calcified bicuspid aortic valve: a calcified pulmonic valve

23. Answer
A. A calcified triscupid aortic valve
without fused commisures; a
normal mitral valve for age

24.  Pulmonary hypertension is most severe in
which untreated valvular disease?
A. Pulmonary stenosis
B. Aortic stenosis
C. Aortic insufficiency
D. Mitral stenosis
E. Mitral insufficiency

25. Answer
 D. Mitral stenosis
Although not usually severe, the commonest forms of pulmonary
hypertension are those that occur secondary to chronic lung
disease and left ventricular failure.
 Thus, pulmonary hypertension and right ventricular hypertrophy
(cor pulmonale) may complicate the course of severe chronic
obstructive pulmonary disease (COPD).
 In addition, any cause of left ventricular failure may lead to
pulmonary venous congestion and hence pulmonary hypertension

Similarly, unidentified mitral stenosis may present with symptoms
of severe right heart failure. Other causes include congenital heart
disease, narrowing of small blood vessels in the lung, pulmonary
(emboli and primary pulmonary hypertension (PPH

26.  Constrictive pericarditis is most likely in
A. Uremia
B. Congestive heart failure
C. Rheumatic fever
D. Myocardial infarction
E. Tuberculosis

27. A body of a 57 year old woman underwent autopsy after she was
run down by the Graham Ambulance Service outside the clinic.
Multiple 2-4 mm vegetations were found on an otherwise normal
mitral valve. the vegetations were made of fibrin on histological
section, and the underlying valve was essentially normal. The
history that would be most likely when you get her clinic chart
A. Long history of intravenous drug abuse with recent history of
fevers to 104 degree F
B. Pancreatic carcinoma being treated on an experimental protocol
for chemotherapy
C. History of rheuthmatic fever at age nine with long term mitral
stenosis and recent onset of fevers to 103 degree F
D. Long history of systemic lupus erythematosis (SLE(

28.  D. Long history of systemic lupus erythematosis (SLE)
 Systemic lupus erythematosus (SLE) is an autoimmune
disease characterized by production of autoantibodies to
parts of the cell nucleus.
 Cardiac complications include pericarditis, endocarditis
(heart murmurs and valvular damage secondary to LIBMAN-
SACKS VEGETATIONS ON THE MITRAL VALVE), and coronary
artery disease (CAD). 50% of SLE patients have endothelial
damage to their heart valves
 Endocarditis in the form of nonbacterial vegetations (Libman
Sacks nodules) vary from mild valvular thickening (common
but with little or no functional problems) to large vegetations
affecting the function of the valve

29.  Severe back pain of acute onset in a 26 year old
woman in her 35th week of gestation for her third
child
A. Takayasu arteritis
B. Giant cell arteritis
C. Aortic dissection
D. Polyarteritis nodosa
E. Wegener's granulomatosis

30.  D. Polyarteritis nodosa
Polyarteritis nodosa (PAN) is a necrotizing systemic
vasculitis involving the wall of small and medium
sized arteries.
 The histologic aspect is defined by the presence of
fibrinoid necrosis and an infiltrate rich in neutrophil
polynuclears in the artery wall and rare granulomas.
 Clinical manifestations are misleading, and more often
the symptoms of the disease are retrospectively
related to the PAN.

31.  Which one of the following is not true about the development
of acute rheumatic fever?
 A. IT DEVELOPS DURING THE ACUTE PHASE OF A GROUP
A BETA-HEMOLYTIC STREPTOCOCCAL INFECTION OF
THE THROAT.
 B. IT IS NOT ASSOCIATEDWITHSTREPTOCOCCAL
INFECTION OF SITES OTHERTHAN THE PHARYNX.
 C. IT USUALLY OCCURS DURING THE COURSE OF
EPIDEMICS OF STREPTOCOCCAL THROAT INFECTIONS
IN CROWDEDSETTINGS.
 D. IT IS FARMORE COMMON IN UNDERDEVELOPED
COUNTRIES THAN IN THE UNITEDSTATES.
 E. ITS LESIONS INVOLVE THE HEART, JOINTS, SKIN AND
NERVOUS SYSTEM

32.  The Correct Answer is A
Acute rheumatic fever is triggered by infection with specific strains of
group A streptococci which possess antigens that cross-react with
human connective tissue, particularly heart valve glycoprotein...
The condition usually affects children or young adults, and
there is a familial variation in susceptibility...its prevalance in
Western Europe and North America has progressively declined
to very low levels, but it remains common in parts of asia, africa
and south america, where it is still the most common cause of
acquired heart disease in childhood adolescence...
Rheumatic fever is a systemic illness typically presenting with
fever, anorexia, lethargy and joint pains...
Arthritis occurs in approximately 75% of patients and other
features include skin rashes, carditis and neurological
features...
Anti-streptococcal antibody, anti-streptolysin antibody, positive
culture for group A streptococcus, recent scarlet fever...
Erythema marginatum (the expanding erythematous rash) and
sydenham chorea (rapid, purposeless movements) also
accompany this disorder...
Carditis is the most important manifestation of rheumatic
fever...carditis presents as breathlessness, palpitations or chest
pain...

33.  Otherfeatures consist of tachycardia, cardiac enlargement and
new orchanged cardiac murmurs...
A soft systolic murmuris common but non-specific...a soft mid-
diastolic murmuris often due to valvulitis, with nodules forming
on the mitral valve leaflets...
There is a pericardial friction rub which is oftenintermittent...
 cardiac failure may result eitherfromimpaired function of
ventricularmuscle orfrommitral oraortic incompetence and
tends to occurin a 'fulminant' formof rheumatic feverthat is
more common in developing countries...
Electrocardiographic changes include ST orT wave changes;
conduction defects sometimes occurand may cause syncope...
Mitral valve becomes thickened with fused chorda tendinea...
Aortic regurgitation occurs...

34.  Complications of rheumatic feverinclude:
 Cardiac arrhythmias
 Pericarditis
 Rheumatic pneumonitis
 Pulmonaryembolism
 Pulmonaryinfarction
 Valvedeformity, andinextremecases, congestiveheart
failure.

35.  The following are causes of prolonged QT
interval except:
A. Romano Ward syndrome
B. Erythromycin
C. Cisapride
D. Hypocalcaemia
E. Hyponatraemia

36.  The most common cardiac malformation
is:
A. Atrial septal defect
B. Endocardial cushion defect
C. Ventricularseptal defect
D. Aortic stenosis

37.  The correct answer is C
 VSD most common CHD(25%), membranous type most
common, large LA/RV, LV remains normal
 ASD
– ostiumsecundumtype most common, large RA/RV/PA ASD;
 PDA premature infants, maternal rubella, large LA/LV/aorta;
ESDostiumprimumASD, Down’s, gooseneckdeformity on
angio fromLV outlet obstruction
 PAPVR– right SVC most common, IVC (scimitarsyndro)
– most common cyanotic Tetralogy of Fallot
stenosis/RVH/VSD/overriding aorta, boot-shaped heart, right
aortic arch in 25%, small orconcave PA;

38.  Which one of the following statements is not true?
 A.THE VEGETATIONS OF INFECTIVE ENDOCARDITIS OFTEN
EMBOLIZE.
 B.THE VEGETATIONS OF NONBACTERIAL THROMBOTIC
ENDOCARDITIS OFTEN EMBOLIZE.
 C.THE VEGETATIONS OF ACUTE RHEUMATIC FEVER OFTEN
EMBOLIZE.
 D.THE VEGETATIONS OF SYSTEMIC LUPUS ERYTHEMATOSUS
(LIBMAN-SACKS DISEASE) LACK EMBOLIC PROPENSITY.
 E.FUNGAL ENDOCARDITIS VEGETATIONS ARE USUALLY VERY
LARGE.

39.  The Correct Answer is C
Small thrombi that develop on cardiac valves are termed vegetations.
Vegetations may be seen in bacterial infection of the valves (bacterial
endocarditis) also seen with IV drug users, systemic lupus
erythematosus, and in chronic wasting states.
 The four major forms of vegetative endocarditis:
A. RHD (Rheumatic Heart Disease) – Notice what looks like a string of
beads which are small verrucae or small vegetations, sterile deposits
of fibrin tend toward a predilection for the closing margin of the valve
(not the free edge). This is where the trauma is occurring as the valve
closes.
B. IE (Infective Endocarditis) – The damage may start on the closing
margin of the valve, particularly if the valve is already damaged.
Unlike RHD, they tend to be larger and bulkier. Particularly with fungal
infective endocarditis as compared to bacterial, the vegetations
become very large. The larger they are, the greater the risk of
breaking off and embolizing.
C. NBTE (non-bacterial thrombotic endocarditis) – tend to be localized
and also tend to be at the closing margin. They can grow large enough
to break off and embolize depending on the circumstances.
D. SLE (Libman-Sacks endocarditis) – Lesions also tend to occur at the
closing margin. One of the distinctive features here is that the
vegetations can be on either or both sides of the valve leaflets (notice
how the artist shows the leaflet partially lifted to demonstrate the
underside of the leaflet.

40.  Troponin T is a sensitive and specific marker
for:
 a. typical angina
b. crescendo angina
c. myocardial infarction
d. arrhythmia
e. Prinzmetal's angina

41.  The correct answer is C
Troponin T is a specific marker of myocardial
ischaemia and is sensitive providing the sample was
taken 16h or more after the suspected cardiac event;
earlier sampling may produce false negative results.
Troponin T may stay elevated for 7-10 days post MI.
In Acute Coronary Syndrome, Trop T >0.1 μg/L
consistent with myocardial infarction; Trop T 0.03 –
0.1 μg/L consistent with minor myocardial damage

42.  Complications of myocardial infarction
include all of the following except:
A. rupture of left ventricle
B. rupture of papillary muscle
C. mural thrombi
D. vasospasm
E. pericarditis

43.  The correct answer is D
Complications of Myocardial Infarction
 RECURRENT CHEST PAIN
 IF POST-MI ANGINA OCCURS (20-30%), PATIENTS
OFTEN GET PTCA OR CABG
 RECURRENT MI (5-20%) WITHIN FIRST SIX WEEKS
CARDIAC ARRHYTHMIAS AND CONDUCTION DEFECTS
(BRADY- AND TACHYARRHYTHMIAS)
 EXTREMELY COMMON W/ MI, MAJOR SOURCE OF
MORTALITY BEFORE PATIENT REACHES HOSPITAL
 Mechanisms
 ANATOMIC INTERRUPTION OF PERFUSION TO STRUCTURES OF
CONDUCTION PATHWAY
 ACCUMULATION OF LOCAL METABOLIC FACTORS AND
ABNORMAL TRANSCELLULAR ION CONCENTRATIONS DUE TO
MEMBRANE LEAKS
 AUTONOMIC STIMULATION
 ADMINISTRATION OF POTENTIALLY ARRYTHMOGENIC DRUGS

44. Types:
 VENTRICULAR FIBRILLATION
 DURING FIRST 48 HOURS PROBABLY RELATED TO ELECTRICAL INSTABILITY
 AFTER FIRST 48 HOURS PROBABLY RELATED TO LV DYSFUNCTION
 SUPRAVENTRICULAR ARRYTHMIAS
 SINUS BRADYCARDIA (EXCESSIVE VAGAL STIMULATION OR SA NODAL ISCHEMIA
 SINUS TACHYCARDIA (PAIN, ANXIETY, CHF, DRUGS, VOLUME DEPLETION)
 ATRIAL PREMATURE BEATS AND ATRIAL FIBRILLATION (ATRIAL ISCHEMIA OR
DISTENSION SECONDARY TO LV FAILURE)
 CONDUCTION BLOCKS
 MAY RESULT FROM ISCHEMIA OR INCREASED VAGAL TONE
 RIGHT VENTRICULAR INFARCTION
 1/3 OF THOSE WITH MI OF LV INFERIOR WALL WILL ALSO GET RV INFACT
B/C BOTH ARE SUPPLIED BY RIGHT CORONARY ARTERY (USUALLY(
 WILL GET SIGNS OF RIGHT SIDED HEART FAILURE INCLUDING JVD,
PROFOUND HYPOTENSION (LV BECOMES UNDERFILLED)
 MECHANICAL COMPLICATIONS, INCLUDING:
 PAPILLARY MUSCLE RUPTURE
 CAN BE RAPIDLY FATAL BECAUSE OF SEVERE MITRAL REGURGITATION
 VENTRICULAR FREE WALL RUPTURE
 MAY OCCUR WITHIN FIRST 2 WEEKS OF MI
 MORE COMMON IN WOMEN AND THOSE WITH A HX OF HYPERTENSION
 RESULTS IN CARDIAC TAMPONADE, PSEUDOANEURYSM (IF RUPTURE IS
INCOMPLETE AND PLUGGED WITH A THROMBUS)
 VENTRICULAR SEPTAL RUPTURE

45. 1. VENTRICULAR SEPTAL RUPTURE
DEVELOP LEFT TO RIGHT SHUNT
PRECIPITATES CHF BY VOLUME OVERLOAD OF PULMONARY
CAPILLARIES
1. VENTRICULAR ANEURYSM
 USUALLY OCCURS WEEKS TO MONTHS AFTER MI AS WALL
PROGRESSIVELY WEAKENS, BUT NOT PEFORATED BY
PHAGOCYTIC CLEARANCE OF NECROTIC TISSUE
 GET LOCALIZED OUTWARD BUGLE WHEN VENTRICLE
CONTRACTS
 RUPTURE AND TAMPONADE DO NOT DEVELOP
 COMPLICATIONS INCLUDE THROMBUS FORMATION,
VENTRICULAR ARRHYTHMIAS, HEART FAILURE
 GET PERSISTENT ST SEGMENT ELEVATION (WEEKS AFTER Q
WAVE MI
1. “PUMP” FAILURE
 IMPAIRED VENTRICULAR CONTRACTILITY AND INCREASED
MYOCARDIAL STIFFNESS BOTH LEAD TO SYMPTOMS OF HEART
FAILURE
 SIGNS AND SYMPTOMS INCLUDE DYSPNEA, PULMONARY RALES, S3
 TREATMENT INCLUDES DIURESIS AND VASODILATOR THERAPY

46.  A patient has persist >2mm ST elevation in V2-6 two
hours following a myocardial inraction, with hypertesnion
of 205/115, he has already been given morphine and
aspirin , what is the next management of choice?
a) IV Nitroglycerine
b) Double-bolus r-PA
c) iv GTN
d) iv streptokinase
e) subcutaneous heparin

47.  The correct answer is A
1) patients with ST-segment elevation, i.e. new ST-segment
elevation at the J point with the cut-off points 0.2mV in
V1through V3and 0.1mV in other leads, or
1) patients without ST-segment elevation, i.e. ST-segment
depression or T wave abnormalities.
 Clinically established myocardial infarction may be defined by
any Q wave in leads V1through V3, or Q wave 0.03s in leads I,
II, aVL, aVF, V4, V5or V6.
 Neither the GISSI-2/International Trials nor the Third
International Study of Infarct Survival(ISIS 3)found a
difference in mortality between the use of streptokinase and
tissue plasminogen activator or anistreplase. Furthermore, the
addition of subcutaneous heparin did not reduce mortality
compared with the use of no heparin.
 However, the GUSTO Trial (Global Utilisation of Streptokinase
and Tissue Plasminogen Activator for occluded coronary
arteries)28 employed an accelerated t-PA (tissue type
plasminogen activator) regimen given over 90min29 rather
than the previously conventional period of 3h. Accelerated t-PA
with concomitant APTT (activated partial thromboplastin time)
adjusted intravenous heparin was reported to result in 10 fewer
deaths per 1000 patients treated. The risk of stroke is higher
with t-PA or anistreplase than with streptokinase.

48.  In the GUSTO trial, there were three additional strokes per
1000 patients treated with accelerated t-PA and heparin in
comparison with streptokinase and subcutaneous heparin, but
only one of these survived with a residual deficit.
 In assessing the net clinical benefit, this must be taken into
account with the reduced death rate in the t-PA group. Several
variants of t-PA have been studied. Double-bolus r-PA
(reteplase) does not offer any advantage over accelerated t-PA
except for its ease of administration. Single-bolus weight-
adjusted TNK-tPA (tenecteplase) is equivalent to accelerated t-
PA for 30-day mortality and associated with a significantly
lower rate of non-cerebral bleeds and less need for blood
transfusion.
 Bolus fibrinolytic therapy may facilitate more rapid
treatment in and out of the hospital and reduce the risk
of medication errors. The choice of fibrinolytic agent will
depend on an individual assessment of risk and benefit,
and also on factors such as availability and cost. For late
treated patients more fibrin-specific agents may be
more effective

49.  Platelet aggregation is only partly inhibited by aspirin and progress has been made
with the development of platelet glycoprotein IIb/IIIa inhibitors, which block the
final pathway of platelet aggregation. Angiographic trials demonstrated that the
combination of GP IIb/IIIa inhibitors with half-dose fibrinolytic and reduced doses
of heparin, induces similar or slightly higher TIMI grade 3 flow rates when
compared with full-dose fibrinolytic alone and is associated with more complete
resolutionof ST-segment elevations, suggesting an improvement in tissue
reperfusion. The clinical benefit and safety of these combinations has been

 tested in two large trials.No reductions in 30-day mortality or intracranial
haemorrhage rates but lower rates of in-hospital reinfarction were observed,
however, at the cost of an increase in (mostly spontaneous) non-cerebral bleeding
complications especially in elderly patients.
 Therefore, the routine use of a reduced dose fibrinolytic with abciximab or other
platelet glyco-protein IIb/IIIa inhibitors cannotbe recommended. Whether this
combination therapy may be beneficial in specific subgroups of patients (for
example those at high risk or those likely to undergo early PCI) needs to be further
evaluated.
 Heparin has been extensively used during and after fibrinolysis, especially with
tissue plasminogen activator. Heparin does not improve immediate clot lysis but
coronary patency evaluated in the hours or days following thrombolytic therapywith
tissue plasminogen activator appears to be better with intravenous heparin. No
difference in patency was apparent in patients treated with either subcutaneous or
intravenous heparin and streptokinase.Prolonged intravenous heparin
administration has not been shown to prevent reocclusion after angiographically
proven successful coronary fibrinolysis. Heparin infusion after tissue plasminogen
activator therapy may be discontinued after 24–48h. Close monitoring of
intravenous heparin therapy is mandatory; aPTT values over 70s are associated
with higher likelihood of mortality, bleeding and reinfarction. Although no
randomized trials have beenperformed, there is evidence from recent trials
suggesting that more frequent monitoring of aPTT and a full weight adjustment of
heparinmay decrease the risk of non-cerebral bleeding complications.


50.  Familial hypertrophic cardiomyopathy is most
likely to be secondary to a mutation in:
a) myosin regulatory proteins
b) myosin binding protein-C
c) Myosin light chains
d) Troponin I
e) Troponin T

51.  The correct answer is B
Molecular genetic research has demonstrated that familial
hypertrophic cardiomyopathy is caused by a mutation in one of
nine genes that encode sarcomere proteins.
 Sarcomeres are the contractile units within the cardiac cells;
these are composed of many proteins that are organized into
thin and thick filaments. These filaments slide with respect to
each other during cardiac contraction.
Mutations in thick filament proteins called cardiac B myosin
heavy chain or cardiac myosin binding protein-C appear to
account for approximately 82% of hypertrophic
cardiomyopathy. Mutations in thin filament proteins cardiac
troponin T and a tropomyosin account for about 13% of
hypertrophic cardiomyopathy. Mutations in two other
sarcomere proteins, the myosin regulatory and essential light
chains are quite rare and contribute less than 5% to
hypertrophic cardiomyopathy. Although these percentages are
only estimates, they indicate that more disease-causing genes
will be identified.
A tenth gene has been identified that is a non-sarcomere
protein (a subunit of protein kinase A) is associated with
individuals who have both hypertrophic cardiomyopathy and
Wolf-Parkinson-White syndrome.

52.  A 42-year-old man with acute renal failure is
confused. His serum potassium is 8.1 mEq/L . The
most likely abnormal ECG finding is
 a) T wave inversion
b) PR interval of 300ms
c) QT interval of 0.4s
d) U wave
e) tall tented T waves test

53.  The correct answer is E
 the earliest ECG evidence of hyperkalemia usually
appears in the T waves The variety of changes
include:
 Increased amplitude and peaking of the T wave
 PR interval prolongation
 QRS interval prolongation Flattening of the P wave.
 A plasma potassium of >6.5mmol/l should be treated
urgently unless it is an artefact. Hyperkalemia may
have a variety of causes: Renal failure; Excess
potassium replacement therapy;Acidosis from any
one of various causes (diabetic ketoacidosis, lactic
acidosis, etc.); Presence of insufficient
corticosteroids (Addison's disease). As in
hypokalemia, there may be a poor correlation
between serum potassium levels and the typical ECG
changes.

54.  Which of the following is most commonly associated with
an increased risk for the development of torsades de
pointes?
a) decreased PR interval
b) decreased QRS duration
c) increased PR interval
d) increased QT interval
e) U waves

55.  The correct answer is D

 There is an increased risk for the development of torsades de
pointes, a potentially fatal arrhythmia, when the QT interval is
prolonged. Roden reviewed the drugs most commonly
implicated in QT prolongation and the clinical factors that
increase the risk of torsades de pointes.
 Medication-induced QT prolongation was first recognized with
the use of quinidine in the 1920s. Roden lists other drugs that
also are implicated in prolongation of the QT interval and may
cause torsades de pointes . Use of these medications, especially
when a congenital QT prolongation syndrome or other clinical
risk factor is present, increases the chance that torsades de
pointes may develop. Because the risk of torsades de pointes is
sufficiently high at typical clinical dosages of sotalol, dofetilide,
and ibutilide, the review author recommends inhospital cardiac
monitoring when therapy with these agents is initiated
 The risk of torsades de pointes is not related linearly to the
degree of QT prolongation, although any drug that prolongs the
QT interval beyond 500 msec is thought to confer an elevated
risk. Heart rate exerts an important effect on the risk for
associated torsades de pointes, with a greater propensity for
developing the arrhythmia when bradycardia is present.


56.  A 21 year old healthy female comes to the clinic with
complaints of intermittent palpitations. These episodes
can last from seconds to minutes and are associated
with lightheadedness, diaphoresis, and occassionally
chest pain. Her ECG is below:

58. What are the ECG finding?
 Normal sinus rhythm
2) Short PR interval and delta waves consistent with Wolff-
Parkinson-White (WPW) syndrome

Explanation: WPW occurs when a person is born with an
"accessory pathway" that can bypass the AV node and conduct
action potentials straight from the atrium to the ventricle.
 Normally, the AV node acts to delay the action potentials created in
the sinus node before they reach the ventricles. This normal delay
is represented by the PR interval (the time it takes for the sinus
nodal action potential, which creates the P wave, to reach the
ventricles and cause ventricular depolarization, which creates the
QRS complex). An accessory pathway can conduct action potentials
very fast without any delay (unlike the AV node). Thus in WPW,
after the sinus node fires creating an action potential, conduction
immediately goes to the ventricles through the accessory pathway
without delay creating a short PR interval (PR interval < 0.12
seconds).
 Since the PR interval is so short, the P wave is very close to the
QRS complex and the two usually blend together making the QRS
complex appear to begin with an upslope. This upslope is called a
"delta wave" which is pathogneumonic for the presence of an
accessory pathway indicating WPW syndome

60. What medications should be avoided in this patient?
AV nodal blocking medications
 WPW occurs when a person is born with an "accessory
pathway" that can bypass the AV node and conduct
action potentials straight from the atrium to the
ventricle.
 Since the accessory pathway has a very short refractory
period, it can conduct impulses from the atria to the
ventricles at very fast rates (> 400 imulses per minute).
If the AV nodal conduction is blocked using the AV nodal
blocking medications, more conduction can occur
through the accessory pathway.
 In certain arrythmias like atrial fibrillation this can
cause the ventricular rate to become dangerously fast.
 A good pneumonic to remember the AV nodal blocking
medications is "ABCD" which stands for Adenosine, Beta-
blockers, Calcium channel blockers, and Digoxin.

61. In your clinic she has one of these episodes and an ECG is
performed

62. What are the ECG #2 findings?
 Narrow complex tachycardia consistent with atrial
fibrillation and WPW syndrome (less likely AVNRT,
although still possible.

63. What medication should be given if the rhythm caused
hemodynamic instability or cardiac arrest?
 Procainamide
Once again the AV nodal blocking medications should not
be used since blocking the AV node allows more impuses to
travel through the accessory pathway thus making the
ventricular rate dangerously fast, often precipitating
ventricular fibrillation which is fatal. Procainamide actually
slows conduction through the accessory pathway while
increasing the conduction through the AV node and is the
treatment of choice in patients with WPW and suspected
atrial fibrillation.
Patients with WPW are also at an increased risk of
developing AV nodal rentry tachycardias (AVNRT) which are
difficult to distinguish from atrial fibrillation on ECG due to
the fast ventricular rate present in both rhythms making it
hard to determine if it is irregular. Adenosine is actually
relatively safe to give if the rhythm is AVNRT since no
conduction is occuring in the accessory pathway as occurs
with the combination of WPW and atrial fibrillation
(remember AVNRT occurs with dual pathways within the AV
node

64.  A 55 year old male with a history of diabetes mellitus
type II and hypertension presents to your clinic and has
the below ECG

66. What are the ECG findings?
 The ECG findings include:
Normal sinus rhythm
Poor R wave progression (PRWP)

67. What is the differential diagnosis of this ECG finding?
 The differential diagnosis for poor R wave
progression (PRWP) includes :
 Old anteroseptal infarct (Q waves in V1 to v3)
Left ventricular hypertrophy
Left anterior fascicular block
Left bundle branch block
Late transition or clockwise rotation of the heart
(normal varient)
Wolff-Parkinson-White

68.  You are the house officer on call for the
telemetry floor and a nurse calls you with an
abnormal rhythm seen on telemetry. The
patient was admitted 2 days previously for a
congestive heart failure exacerbation. He
denies any symptoms including chest pain,
palpitations, lightheadedness, or shortness of
breath. Vital signs are normal. You ask for a
12-lead ECG which is below:

70. What are the ECG finding?
 The ECG findings include:
Normal sinus rhythm
 Prominent U waves
A "U wave" occurs just after the T wave and
significantly before the following P wave. U waves can
at times be mistaken for atrial flutter waves or
additional P waves indicating AV block. Also, if the U
wave overlaps with the T wave it may mimic a
prolonged QT interval
.

72. What is the electrophysiologic mechanism responsible for
the findings in the above ECG?
 Prolonged depolarization of a portion of the
ventricles
It is though that a special subpopulation of myocardial
cells exists in the mid-myocardium that has longer action
potentials and longer repolarization times.
 With the presence of specific stressors (hypokalemia,
bradycardia, digoxin use, or LVH), amplitude of the T
wave in the special subpopulation of myocardium with a
longer repolarization times increases.
 Since this repolarization time is significantly longer than
normal myocardium (in which repolarization creates the
T wave), a distinct wave after the T wave is produced
which is called the U wave.

73. You go back to sleep and are soon called again for another abnormal
rhythm seen on the same patient which is intermittently occurring.
The patient is still asymptomatic and vital signs are still normal.
Another 12-lead ECG is obtained which is below

74. Dx
 The ECG findings include:
Normal sinus rhythm
Non-sustained monomorphic ventricular tachycardia
with a rate of slightly less than 300.
 Non-sustained ventricular tachycardia (NSVT) can occur for
multiple reasons, however it is very commonly seen in
patients with systolic congestive heart failure.
 Short runs of NSVT are usually asymptomatic, however
if the NSVT becomes sustained it can be life-threatening.
 Sustained ventricular tachycardia is usually defined as
VT lasing for more than 30 seconds. VT can be
monomorphic (most common) or polymorphic (a.k.a.
Torsades de Pointes(

75. TX
 Replace electrolytes and consider defibrillator
placement if criteria met
 NSVT alone is not life-threatening, however it predicts
an increased risk of sudden cardiac death.
 Correcting electrolyte abnormalities or
revascularizing the treat ischemia significantly
reduces the VT.
 Evidence supports the implantation of automated
implanted cardiac defibrillators (AICDs) in all patients
with systolic congestive heart failure with an ejection
fraction of < 35%.
 An AICD can quickly electrically cardiovert a patient
should sustained VT occur.

76. 45year-old man with a strong family history of ischaemic
heart disease presents with atypical chest pains. Stress
echocardiography is organised. What pharmacologic
agent is likely to be used produce cardiovascular stress
during Stress echocardiography in this patient?
a) dipyridamole
b) Dobutamine
c) adenosine
d) arbutamine
e) Atropine sulfate

77.  The correct answer is A
Explanation
 Stress echocardiography has been developed in recent years as an
effective noninvasive test for the detection and assessment of coronary
artery disease. This method combines exercise with 2-dimensional
echocardiography, which can assess regional and global left ventricular
function during stress.
 Dobutamine infusion, a pharmacologic means of producing
cardiovascular stress, appears to be an excellent alternative to exercise in
echocardiographic studies. Currently, it is reserved for patients who
cannot exercise at a meaningful level because of advanced age, physical
deconditioning, or other factors.
 Dobutamine infusion is the method used most often for pharmacologic
stress echocardiography. Graded dobutamine infusion--10 to 40
micrograms/kg per minute in 3-minute stages--increases myocardial
oxygen demand in a fashion similar to that of staged exercise. During the
dobutamine infusion, it is apparent that heart rate, contractility, and
blood pressure are increased. Dobutamine has the advantage of rapid
onset of action, and its effects can be reversed by giving an intravenous
beta-blocker.
 A synthetic catecholamine that has a relatively short half-life (about 2
minutes) , dobutamine has strong agonist activity at the beta1 receptor
and mild agonist activity at the beta2 and alpha1 receptors.
 Atropine sulfate can be used to increase heart rate, if necessary, and is usually
administered at the peak dobutamine dose. It is usually given as a 0.5-mg bolus and
in 0.25-mg increments every 60 seconds (maximum dose, 1-1.5 mg) until the
desired heart rate is achieved.
Dobutamine infusion is stopped after images are acquired at peak heart rate--or
sooner if the patient has tachyarrhythmias.

78.  A 65 year old male with end-stage COPD gets admitted
to the ICU with respiratory failure. He was found to
have the below ECG

80. DX
 The ECG findings include:
Multifocal atrial tachycardia (three distinct P wave
morphologies)
Incomplete right bundle branch block
Poor R wave progression
PVCs
Multifocal atrial tachycardia (aka MAT) is an irregularly irregular,
tachycaric rhythm in which many foci in the atium chaotically fire
acting as the pacemaker of the heart instead of the sinus node.
The atrial rate is not as fast as in atrial flutter or atrial fibrillation,
so normal AV synchrony can occur. When the rhythm has 3 distinct
P wave morphologies and the heart rate is not fast, the term
"wandering atrial pacemaker" or WAP is used.

81. TX
 The treatment of multifocal atrial tachycardia is
aimed at the underlying cause.
 In our case it would be to treat the COPD
exacerbation and respiratory failure.
 The only medication that has been used to
treat MAT is verapamil with only marginal
success.
 No anticoagulation is needed for MAT in
contrast to atrial flutter/fibrillation since the
atrium are contracting well, but simply
originating in different areas.

82.  Hemoptysis, hematuria and recent nosebleeds in a 43
year old man:
A. Takayasu arteritis
B. Giant cell arteritis
C. Aortic dissection
D. Polyarteritis nodosa
E. Wegener's granulomatosis

83.  E. Wegener's granulomatosis
 This condition is uncommon and occurs in young and
middle aged adults, with a slight male predominance.
The vessels mainly involved in this disease are the
small arteries and veins. Necrotizing granulomatous
lesions of the respiratory tract, focal segmental
glomerulonephritis and vasculitis of other organs
characterizes this condition.

Presenting features include non-specific findings
such as fever, weight loss
 myalgias, arthralgias, malaise and chronic rhinitis or
sinusitis. Supportive otitis, mastoiditis, hearing loss
and a saddle-nose defect may occur.

84.  Jones criteria for the diagnosis of acute rheumatic fever
include major and minor criteria. In the presence of
evidence of a preceding group A streptococcal infection,
which one of the following statements is correct?
 a. the diagnosis requires the presence of one major
criterion only.
 b. the diagnosis requires the presence of at least
three major criteria.
 c. the diagnosis requires the presence of two major
or one major and two minor criteria.
 d. three minor criteria alone are sufficient for the
diagnosis.
 e. two major criteria in the absence of minor criteria
are insufficient for the diagnosis

85.  The correct answer is C
For Diagnosis of Rheumatic fever, two major criteria or one
major and two minor criteria must be present.
 * Major Jones Criteria (manifestations) of Rheumatic fever
. Carditis
. Polyarthritis
. Chorea
. Erythema marginatum
. Subcutaneous nodules
 * Minor Jones criteria of Rheumatic fever:
Clinical:
- Previous rheumatic fever or rheumatic heart disease
- arthralgia
- Fever
Laboratory
-↑Erythrocyte sedimentation rate (ESR)
-↑C-reactive protein

86.  A patient develops an acute febrile illness with shivers,
nonproductive cough, and pleuritic chest pain. Five days
later, he presents to the emergency room after abruptly
having "coughed up" nearly a cup of
blood-stained sputum. Which of the following is most likely
to be seen on chest x-ray?
A. A cavity with a fluid level
B. Blunting of diaphragmatic costal angles
C. Complete opacification of one lobe with no additional
findings
D. Patchy consolidation centered on bronchi
E. Prominent bronchi that can be followed far out into the
lung fields

87.  The correct answer is A.
This is a classic presentation of a pulmonary abscess.
Chronic courses with less severe symptoms (with intermittent
improvement following short courses of antibiotics) are
also sometimes seen, particularly if the diagnosis was not
suspected.
Chest x-ray typically shows pneumonic opacification in which a
cavity, often with a fluid level, is visible.
Pulmonic abscesses can be caused by anaerobes (most
common, particularly if aspiration initiated the abscess),
gram-negative aerobic bacilli, and Staphylococci.
Therapy is based on the organisms isolated, and should be
continued for at least 4 to 6 weeks.
In cases that fail to resolve, the possibility of coexisting
carcinoma should be considered.
Choice B is the x-ray appearance of pleural effusion.
Choice C is the x-ray appearance of lobar pneumonia.
Choice D is the x-ray appearance of bronchopneumonia.
Choice E is the x-ray appearance of bronchiectasis.

88.  Which congenital heart disease is most likely to
have hypertrophic and dilated bronchial arteries
as a compensatory mechanism?
a. ventricular septal defect
b. aortic stenosis
c. atrial septal defect
d. persistent truncus arteriosus
e. tetralogy of Fallot

89.  The Correct Answer is E
 In T.O.F.
Roentgenogrophic examination characteristically reveals a
normal-sized, boot-shaped heart (“coeur en sabot”) with
prominence of the right ventricle and a concavity in the region
of the underdeveloped right ventricular outflow tract and main
pulmonary artery.
The pulmonary vascular markings typically are diminished, and
the aortic arch and knob may be on the right side; the
ascending aorta usually is large. A uniform, diffuse, fine
reticular pattern of vascular markings is noted in the presence
of prominent collateral vessels .
The degree of obstruction to pulmonary blood flow is the
principal determinant of the clinical presentation. The site of
obstruction is variable. Infundibular stenosis is the only major
obstruction in about 50% of patients and coexists with valvular
obstruction in another 20 to 25 per cent.
Supravalvular and peripheral pulmonary arterial narrowing may
be observed, and unilateral absence of a pulmonary artery
(usually the left) is found in a small number of patients.
Circulation to the abnormal lung is accomplished by bronchial
and other collateral arteries.

90. THANKS FOR YOUR PATIENTS
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