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Cardiology Jipmer PDF
Cardiology Jipmer PDF
A.60 mg
B.180 mg
C.90 mg
D.300 mg
A.180 mg
B.60 mg
C.90 mg
D.300 mg
A. 6 to 9 hrs
C. 2 to 6 hr
A. Aortic Dissection
C. Menses
B. Previous IC Bleed
C. Dementia
A MC mutation is calmodulin
B. Precipitation by swimming
D. Causes bidirectional VT
C. Quinidine is used
D. Related to SIDS
A. Orthodontic Transplant
B. Manipulation of Gingiva
A. Dyslipedemia
B. Hypertension
C. DM
D. Syndrome X
A. All
B. Outflow VT
D. Atrial fibrillation
A. ACE inhibitors
B. ARB
C. B blocker
D. Diuretics
B. TAPVC
C. HLHS
D. TA
C. Useful in Refractory VT
A MS MR
B MS AR
C. MS AS
D. MR AS
A. Wide QRS
B. Tall T wave
C. Decreased P wave
D. Short PR
A. Typical AVNRT
B. AVRT
C. Atypical AVNRT
D. PJRT
A. Janeway
B. Rose spots
C. Osler node
D. ICH
A. Janeway
B. Osler node
C. Pulmonary embolism
D. IC bleed
A. Alteplase
B. Reteplase
C. Tenecteplase
D. STK
A. Tenecteplase
B. Alteplase
C. Reteplase
D. STK
22.50 years old male which of the following antihypertensive isn't first line treatment
A. B blocker
B. ARB
C. Diuretic
D. CCB
23. Time for FMC to device is 150 min what will be your line of management
A. Thrombolyse
B. PCI
C. Coronary vasodilator
D. Observation
24. 35 years old male present with chest pain and ST elevation and died shortly the Type of MI is
A. Type 3
B. Type 2
C. Type 4a
D. Type 4b
B. LCX
C. RCA
D. LMCA
A. Fondaparinux
B. Bivalirudin
C. UFH
D. LMWX
B. MC is right
C. MC is total absence
D. Diagnosed on X ray
29. In thermodilution method of CO measurements, which of the following isn't required to calculate
A. Volume of injection
B. Specific gravity
C. Temperature of injection
D. Rate of injection
30. Fingerised thumb A/W
B. Marfan
C. Noonans Syndrome
D. Williams Syndrone
A. EAD
B. DAD
C. Rentry
D. Automaticity
A. DAD
B. EAD
C. Reentry
D. Automaticity
1. Valvular AS
2. Supra valvular AS
3. Sub valvular AS
A. 1>2>3
B. 2>3>1
C. 1>3>2
D. 3>2>1
A. ALCAPA
B. Ebstein
C. TGA
D. Single ventricle
A. NYHA grade 1
B. Atrial fibrillation
C. EF less than 30 %
A. Hepatojugular reflux
B. Hepatomegaly
C. Rales
D. JVP
C. The most common reason for failure to wean a heart transplant recipient from cardiopulmonary
bypass is right-sided heart failure
D. The incidence of hypertension may be lower with tacrolimus than with cyclosporine.
A. S3
B. Rales
C. JVP
D. Peripheral edema
A. 45 %
B. 55 %
C. 65 %
D. 75 %
B. Delayed S1
C. Diastolic MR is seen
A. Quinidine
B. Digoxin
C. Verapamil
D. Aldactone
42. SAN potential is
A. - 40 to - 60
B. - 90
C. - 60 to – 80
D. -70
A. Paroxysmal
B. Persistent
C. Longstanding persistent
D. Permanent
A. Sensitivity
B. NPV
C. PPV
D. Specificity
A. RCM
B. DCM
C. HCM
D. Cardiac amyloidosis
46. Patient with lymph edema, webbed neck, pulmonary stenosis diagnosis expected is
A. Turner syndrome
B. Down syndrome
C. Cri-du-Chat syndrome
D. Noonans syndrome
A. Obesity
B. Renal failure
C. Heart failure
D. Advanced age
A. Reentry
B. Triggered activity
C. Early deplorisation
D. Delayed deplorisation
A LMWH
B LEPIRUDIN
C UFH
D ARGATROBAN
50. In a patient suspected MI first aid treatment is
A. Clavix
B. Avas
C. Sorbitrate
D. LMWH SC
A. Systolic bruit
A. 1
B. 2
C. 3
D. 4
54. Old age with aortic area 1.2 cm2. Severity of AS is
A. Severe AS
B. Moderate AS
C. Mild AS
D. Critical AS
A. Dominate RV at birth
57. 10 year old boy with severe PS. ECG shows R wave 22mm in V1. What is RVSP?
A.12 mmHg
B. 110
C. 220
A. rS in 2,3,aVF
B. LAD
C. Deep S in V4,5,6
B. Innominate vein
A. Ten percent to 15% of ostium secundum atrial septal defects are associated with partial anomalous
pulmonary venous connections
B. Eighty percent to 90% of superior vena caval sinus venosus defects are associated with anomalous
connection of the right superior pulmonary vein to the right atrium or superior vena cava
C. About 90% of partial anomalous pulmonary venous connections join the left upper or middle lobe
pulmonary veins into the right atrium or superior vena cava
A. Common atrium
B. Cortriatrium
C. Ebstein
C. In PAPVC with intact septum flow in anomalous drained lung will be increased
B. Notch p wave in 2
B. MR
C. MI
D. Stroke
66. Can't be ruled out commonly in TOF and DORV with VSD with PS is
A. ESM
B. Thrill
D. Parasternal heave
A. Ca channelopathy
B. Quinidine is treatment
B. Antidromic AVRT
C. Short PR interval
C. Noninvasive test
A. Long QT syndrome
B. Brugada syndrome
C. TDP
D. Left septal VT
A. Class IA
B. Class II
C. Digitalis
D. Class IC
ANSWERS
1. A, 2.A ,3.B ,4.A ,5.C ,6.A ,7.B ,8.B ,9.B ,10.A ,11.B ,12.A ,13.C , 14.A ,15.A ,16.D ,17.A ,18.C ,19.B ,20.B
,21.B ,22.A ,23.A ,24.A ,25.B ,26.A ,27.A ,28.A ,29.D ,30.A ,31.A ,32.A ,33.C ,34.A ,35.A ,36.A ,37.A ,38.B
,39.C ,40.B ,41.B ,42.A ,43.B ,44.A ,45.C ,46.D ,47.A ,48.A ,49.B ,50.A ,51.D ,52.C ,53.B ,54.B ,55.C ,56.A
,57.B ,58.B ,59.C ,60.D ,61.C ,62.D ,63.C ,64.A ,65.B ,66.A ,67.B ,68.C ,69.D ,70.C ,71.D ,72.D
EXPLANATIONS
In valvular aortic stenosis, pulse pressure (P-P) is increased on the first beat after the premature
ventricular complex (PVC). In HCM, the opposite is observed.
Adenosine may be useful to help differentiate among causes of wide-QRS tachycardias because it
terminates many SVTs with aberrancy or reveals the underlying atrial mechanism and does not block
conduction over an accessory pathway or terminate most VTs. In rare cases, however, adenosine
terminates some VTs, characteristically those of right ventricular outflow tract origin as noted earlier,
and therefore tachycardia termination is not completely diagnostic of an SVT.
12. Answer. A (Go through books – Quick review of clinical trials in cardiology and cardiac drugs and
their trials for all trials)
Mexiletine does not appear to affect human atrial muscle. It does not affect the QT interval. It has been
used in treating a variety of other disorders, including erythromelalgia (red, painful extremities) in
children and myotonia.
Normally, mexiletine is eliminated metabolically by the liver, with less than 10% being excreted
unchanged in urine. Doses should be reduced in patients with cirrhosis or left ventricular failure. Renal
clearance of mexiletine decreases as urinary pH increases.
15. Answer. A (Braunwald 11th online edition 897, Essentials of clinical cardiology 3473, Essentials of
clinical cardiology 191)
The predominant cause of mitral stenosis (MS) is rheumatic fever,with rheumatic changes present in
99% of stenotic mitral valves excised at the time of mitral valve replacement. Approximately 25% of all
patients with rheumatic heart disease have isolated MS, and approximately 40% have combined MS and
mitral regurgitation (MR). Multivalve involvement is seen in 38% of patients with MS, with the aortic
valve affected in approximately 35% and the tricuspid valve in approximately 6%. The pulmonic valve is
rarely affected.
16. Answer. D (Braunwald 11th online edition 348, Essentials of clinical cardiology 104)
Progressive extracellular hyperkalemia reduces atrial and ventricular resting membrane potentials,
thereby inactivating sodium channels, which decreases Vmax and conduction velocity. The QRS begins
to widen, and P wave amplitude decreases. PR interval prolongation can occur, followed sometimes by
second- or third-degree atrioventricular block. Complete loss of P waves may be associated with a
junctional escape rhythm or putative sinoventricular rhythm. In the latter, sinus rhythm persists with
conduction (possibly over internodal tracts or muscle bundles) between the sinoatrial and
atrioventricular nodes, but without producing an overt P wave.
1
20. Answer. B (Braunwald 11th online edition 2778)
Type 3: Myocardial Infarction Resulting in Death When Biomarker Values Are Unavailable
Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic changes
on the ECG or new LBBB, but death occurring before blood samples could be obtained, before cardiac
biomarkers could rise, or in rare cases, when cardiac biomarkers were not collected.
25. Answer. B
Coronary artery involvement: Coronary ectasia or dilatation is recognized in 50 % of patients during the
acute stage. An aneurysm is defined as a segment whose internal diameter is ≥ 1.5 times the adjacent
segment. About 15 to 20 % of untreated patients and 5% of those treated with IVIG develop coronary
artery aneurysms. They usually occur within 1 to 3 weeks (mean 10 days) and if they are not involved
during this period, it is extremely unusual for them to be affected subsequently. They are classified
(American Heart Association) based on their internal diameter as small (< 5 mm), medium (5-8 mm) or
giant (≥ 8 mm).10 The Japanese Ministry of Health considers coronary arteries as abnormal if the
internal lumen diameter is > 3mm in children < 5 years old or > 4 mm in children ≥ 5 years old, or if the
lumen is irregular. They are called fusiform, when they have a dominant longitudinal dilation and
saccular, when their transverse axial and lateral diameters are nearly equal. The most frequent site for
aneurysm formation is the proximal LAD and proximal RCA, followed by the left main coronary artery
(LMCA), the left circumflex artery (LCX), and finally the distal RCA and the junction between the RCA and
the posterior descending coronary artery. Giant coronary aneurysms occur in less than 1% of cases and
are usually associated with a greater morbidity and mortality due to increased risk of rupture,
thrombotic occlusion or stenotic obstruction leading to myocardial infarction. In a 10- to 21- year follow-
up study by Kato et al,9 46% of giant coronary aneurysms developed stenosis or complete obstruction
and 67% experienced myocardial infarction, with a 50% mortality rate. Fusiform aneurysms tend to have
a better outcome than the saccular ones.
The necropsy incidence rate of congenital absence of the pericardium has been estimated at 1/14,000.9
About two thirds of cases are represented by partial absence of the left pericardium. Congenital absence
of the right pericardium is rare. Approximately one third of congenital pericardial defects occur in
conjunction with other congenital malformations, both cardiac and noncardiac.
Because CPVT is associated with bidirectional, broad-complex ventricular tachycardia, it has been
suggested that the arrhythmogenic mechanism is analogous to that observed in digitalis intoxication
(i.e., calcium overload-induced delayed after depolarizations).
ALCAPA (Anomalous Left Coronary Artery from the Pulmonary Artery) has been used as a general
designation, but the ALCA does not include an anomalous right coronary artery and the PA does not
distinguish the pulmonary trunk from its right or left branch. In this chapter, the designation anomalous
origin of the left coronary artery from the pulmonary trunk applies to the most prevalent variation, and
the less or least prevalent variations are described individually.
The anomalous left coronary artery is a thin-walled vessel that resembles a venous channel. The right
coronary artery originates from its normal aortic sinus, is dilated and tortuous
(As it becomes some sort of left to right shunt from aorta to RCA to collaterals to LAD to pulmonary
artery, to perfuse more blood LV – RCA dilates)
In the absence of parasympathetic innervation, which normally lowers the heart rate, the resting heart
rate of a recipient typically is 90 to 115 beats/min. Likewise, beta blockers may further impair exercise
response in the transplant recipient and should not be given as first-line agents for treatment of
hypertension in this group.
The peripheral signs of AR are often not impressive and certainly not as dramatic as in patients with
chronic AR. The normal or only slightly widened pulse pressure may lead to significant underestimation
of the severity of the valvular lesion. The LV impulse is normal or almost normal, and the rocking motion
of the chest characteristic of chronic AR is not apparent. S1 may be soft or absent because of premature
closure of the mitral valve, and the sound of mitral valve closure in mid- or late diastole occasionally is
audible.
Closure of the mitral valve may be incomplete, however, and diastolic MR may occur.
The early diastolic murmur of acute AR is lower-pitched and of shorter duration compared with that of
chronic AR, because as LV diastolic pressure rises, the (reverse) pressure gradient between the aorta
and left ventricle is rapidly reduced. A systolic murmur is common, resulting in to-and-fro sounds. The
Austin Flint murmur often is present but is of brief duration and ceases when LV pressure exceeds left
atrial pressure in diastole.
A short QT interval on an ECG without a family history of SCD or a history of syncope, palpitations, or AF
may not necessarily indicate an increased risk for SCD, and similarly, some patients with known SQTS
mutations have QT intervals in the lower range of normal. Patients often have persistently short QT
intervals, short or absent ST segments, and tall and narrow T waves in the precordial leads. Other causes
of SQTS, such as hyperkalemia, hypercalcemia, hyperthermia, acidosis, and digitalis, should be excluded.
42. Answer. A (Braunwald 11th online edition 1548)
Atrial fibrillation that terminates spontaneously within 7 days is termed paroxysmal, and AF present
continuously for more than 7 days is called persistent. AF that persists for longer than 1 year is termed
longstanding persistent, whereas longstanding AF refractory to cardioversion is termed permanent.
However, permanent AF is not necessarily permanent in the literal sense because it may be successfully
eliminated by surgical or catheter ablation. Some patients with paroxysmal AF occasionally can have
episodes that are persistent, and vice versa.
A confounding factor in the classification of AF is cardioversion and antiarrhythmic drug (AAD) therapy.
For example, if a patient undergoes transthoracic cardioversion 24 hours after AF onset, it is unknown
whether the AF would have persisted for more than 7 days. Furthermore, AAD therapy can change
persistent AF into paroxysmal AF. It is generally thought that the classification of AF should not be
altered on the basis of the effects of electrical cardioversion or AAD therapy.
Reentry is regarded as the dominant mechanism in Brugada syndrome, based on: conduction slowing,
easy VT/VF induction during EPS, and the polymorphic nature of the arrhythmias.
Although polymorphic tachycardias and tachycardia onset during slow heart rates are also compatible
with EADs, EADs typically require QT prolongation, which is, however, not present in Brugada syndrome;
furthermore, quinidine's efficacy in preventing tachyarrhythmias, while also causing QT prolongation,
argues against a causative role of EADs.
DADs are even less likely: DADs typically occur during calcium (Ca) overload, e.g., fast heart rates.
Attenuation of ST elevations by catecholamines provides further evidence against DADs, as
catecholamines generally increase Ca overload and facilitate DADs.
Finally, abnormal automaticity does not usually present as a polymorphic tachycardia and exhibits a
warm-up phenomenon, rather than the abrupt tachyarrhythmia onset seen in Brugada syndrome.
Lepirudin has a plasma half-life of 60 minutes after intravenous infusion and is cleared by the kidneys.
Consequently, lepirudin accumulates in patients with renal insufficiency. Antibodies against the drug
develop in a high proportion of lepirudin-treated patients. Although these antibodies rarely cause
problems, in a small subset of patients they can delay lepirudin clearance and enhance its anticoagulant
activity; some of these patients experience serious bleeding.
51. Answer. D (Braunwald 11th online edition 858)
The typical presentation is groin tenderness, a palpable pulsatile mass, and a systolic bruit. Sizes less
than 2 cm represent a low likelihood of rupture and may be followed clinically with serial ultrasound to
document spontaneous thrombosis. For pseudoaneurysms larger than 2 cm in size, ultrasound-guided
manual compression with or without thrombin or collagen injection is the treatment of choice. Covered
stent placement or surgery are rarely required.
The ECG frequently shows low-voltage limb leads, often with an unusually rightward axis. First-degree
AV block is common, and Q waves are frequently seen in leads V1 to V3. Left bundle branch block is rare
in AL amyloidosis
CMR is a useful diagnostic tool for all forms of cardiac amyloidosis. The classic features of cardiac
amyloidosis include biventricular thickening with normal cavity size, as well as atrial septal thickening.
With the use of gadolinium, there is often difficulty in nulling the myocardium, and late gadolinium
enhancement typically shows diffuse or patchy subendocardial enhancement, which often involves the
atrium. This combination of findings is unusual in other cardiomyopathies and strongly suggests cardiac
amyloidosis.
Severe obstruction to LV outflow usually is characterized by the following: (1) an aortic jet velocity of 4
m/sec or greater; (2) a mean transvalvular pressure gradient at least 40 mm Hg in the presence of a
normal flow; or (3) an effective aortic orifice no greater than 1.0 cm2 in an average-sized adult (i.e., ≤0.6
cm2/m2 of body surface area), which is approximately 25% of the normal aortic orifice of 3.0 to 4.0 cm2.
Moderate AS is characterized by an aortic jet velocity of 3.0 to 3.9 m/sec or mean transvalvular pressure
gradient of 20 to 39 mm Hg, usually with an aortic valve orifice area (AVA) of 1.0 to 1.5 cm2.
Mild AS is characterized by an aortic jet velocity of 2.0 to 2.9 m/sec or mean transvalvular pressure
gradient less than 20 mm Hg, usually with aortic orifice of 1.5 to 2.0 cm2
b. All the durations and intervals (PR interval, QRS duration, and QT interval) are shorter than in the
adult.
c. The RV dominance of the neonate and infant is expressed in the ECG by the following:
(2) Large rightward forces (tall R waves in aVR and the right precordial leads [RPLs, i.e., V4R, V1, and V2]
and deep S waves in lead I and the left precordial leads [LPLs, i.e., V5 and V6]).
(3) The R/S ratios in the RPLs are large and those in the LPLs are small. The R/S ratio is the ratio of the R
amplitude and the S amplitude in a given lead.
d. The T wave is inverted in V1 in infants and small children with the exception of the first 3 days when
the T waves may be normally upright.
Arterial
Bidirectional cavopulmonary (Glenn) shunt (end-to-side SVC to LPA and RPA shunt)
LPA, left PA; PA, pulmonary artery; RPA, right PA; SVC, superior vena cava.
Initial activation of the interventricular septum is oriented from left to right in the frontal plane and
anteriorly in the horizontal plane, corresponding to the anatomic position of the septum within the
chest.
This wavefront produces an initial positive wave in leads with axes directed to the right (lead aVR) or
anteriorly (lead V1). Leads with axes directed to the left (leads I, aVL, V5, and V6) will register initial
negative waves known as septal q waves. These initial forces are normally of low amplitude and are brief
(<30 msec in duration). The absence of these septal q waves, with QS complexes evident in the right
precordial leads or with initial R waves in leads I, V5, and V6, is a common normal variant and not
associated with any specific cardiac disease.
59. Answer. C (Braunwald 11th online edition 314, Essentials of clinical cardiology 102)
Frontal plane mean QRS axis between −45 and −90 degrees
Frontal plane mean QRS axis between +90 and +180 degrees
rS pattern in leads I and aVL with qR patterns in leads III and aVF
Exclusion of other factors causing right axis deviation (e.g., right ventricular overload patterns, lateral
infarction)
The so-called figure-of-8, or snowman, heart is due to enlargement of the heart and the presence of a
dilated right superior vena cava, innominate vein, and left vertical vein.
Partial anomalous pulmonary venous connection refers to one or more but not all pulmonary veins that
connect anomalously to the right atrium. Total anomalous pulmonary venous connection exists when all
four pulmonary veins connect anomalously to the right atrium, directly or indirectly. Ten percent to 15%
of ostium secundum atrial septal defects are associated with partial anomalous pulmonary venous
connections. Eighty percent to 90% of superior vena caval sinus venosus defects are associated with
anomalous connection of the right superior pulmonary vein to the right atrium or superior vena cava.
About 90% of partial anomalous pulmonary venous connections join the right upper or middle lobe
pulmonary veins into the right atrium or superior vena cava. Partial anomalous connection of right
pulmonary veins is usually associated with ostium secundum atrial septal defects, exceptionally is
associated with an intact atrial septum, and may go unrecognized when associated with a restrictive
sinus venosus defect. Anomalous connection of left pulmonary veins is far less prevalent (incidence rate
about 10%) than anomalous connection of right pulmonary veins and is represented by anomalous
connection to the innominate vein or to a persistent left superior vena cava that attaches to the
innominate vein. Bilateral partial anomalous pulmonary venous connections are rare.
The scimitar syndrome, described in 1836 by Chassinat, is a rare anomaly characterized by connection of
all of the right pulmonary veins into the inferior vena cava. The ipsilateral lung and pulmonary artery are
usually hypoplastic
62. Answer. D (Braunwald 11th online edition 3788, Essentials of clinical cardiology 109)
A sinus rhythm or atrial fibrillation or flutter may be present. The QRS axis is typically rightward in
secundum ASD and PAPVD/PAPVC, and there may be crochetage of the QRS complex in the inferior
leads. Negative P waves in the inferior leads indicate a low atrial pacemaker often seen in superior sinus
venosus defects, which are located in the area of the sinoatrial node and render it deficient. Complete
right bundle branch block appears as a function of age. Tall R or R′ waves in V1 suggest pulmonary
hypertension.
The physiologic consequences of an atrial septal defect with partial anomalous pulmonary venous
connection are similar if not identical to those of an isolated atrial septal defect with an equivalent net
shunt because the hemodynamic fault remains the left-to-right shunt at atrial level. However, flow
through anomalous pulmonary veins into the right atrium is obligatory and is therefore established
earlier than shunt flow across an atrial septal defect. When partial anomalous pulmonary venous
connection occurs with an intact atrial septum, flow is increased in the segment of lung with the
anomalous pulmonary veins because right atrial pressure is lower than left atrial pressure (intact atrial
septum).The pressure gradient across the anomalously draining lung is therefore greater than across the
normally draining lung.
64. Answer. A (Braunwald 11th online edition 302, Essentials of clinical cardiology 100)
Right posteroseptal accessory pathway - Negative delta waves in leads II, III, and aVF, upright in I and
aVL, localize this pathway to the posteroseptal region. The negative delta wave in V1 with sharp
transition to an upright delta wave in V2 pinpoints it to the right posteroseptal area.
Left lateral accessory pathway - A positive delta wave in the anterior precordial leads and in leads II, III,
and aVF, positive or isoelectric in leads I and aVL, and isoelectric or negative in leads V5 and V6 are
typical of a left lateral accessory pathway.
Right free wall accessory pathway - The predominantly negative delta wave in V1 and the axis more
leftward indicate the presence of a right free wall accessory pathway.
Intracardiac Echocardiography
Left septal VT can be started by rapid atrial or ventricular pacing and sometimes by exercise or
isoproterenol. The prognosis is generally good. RF catheter ablation is effective in symptomatic patients.