CARDIOVASCULAR

SYSTEM
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 DEVELOPMENT OF CARDIOVASCULAR SYSTEM 1
CARDIOVASCULAR SYSTEM

CONTENTS
DEVELOPMENT OF CARDIOVASCULAR SYSTEM ............................................................................................................ 6
ANATOMY OF CARDIOVASCULAR SYSTEM ................................................................................................................... 6
PHYSIOLOGY OF CARDIOVASCULAR SYSTEM ................................................................................................................ 7
GENERAL FEATURES OF PHYSIOLOGY OF CARDIOVASCULAR SYSTEM ..................................................................... 7
OXYGEN CONSUMPTION......................................................................................................................................... 10
MEAN ARTERIAL PRESSURE .................................................................................................................................... 10
PULSE PRESSURE ..................................................................................................................................................... 11
VASCULAR SYSTEM ..................................................................................................................................................... 11
SYNCOPE ..................................................................................................................................................................... 12
HEART SOUNDs ........................................................................................................................................................... 12
FIRST HEART SOUND ............................................................................................................................................... 12
SECOND HEART SOUND .......................................................................................................................................... 12
THIRD HEART SOUND .............................................................................................................................................. 13
FOURTH HEART SOUND .......................................................................................................................................... 13
SNAP, CLICK AND THRILL ......................................................................................................................................... 13
MURMUR ................................................................................................................................................................ 14
ARTERIAL PULSE AND JUGULAR VENOUS PULSE ........................................................................................................ 14
GENERAL FEATURES OF PULSE ................................................................................................................................ 14
PULSUS BISFERIENS ................................................................................................................................................. 15
PULSUS PARADOXUS ............................................................................................................................................... 15
PULSUS ALTERANS .................................................................................................................................................. 15
JUGULAR VENOUS PULSE ........................................................................................................................................ 15
ELECTROCARDIOGRAM ............................................................................................................................................... 16
GENERAL FEATURES OF ECG ................................................................................................................................... 16
ECG FEATURES OF HYPERKALEMIA ......................................................................................................................... 17
ECG FEATURES OF HYPOKALEMIA .......................................................................................................................... 17
ECG FEATURES OF HYPERCALCEMIA ....................................................................................................................... 17
ECG FEATURES OF HYPOCALCEMIA ........................................................................................................................ 17
ANGINA ....................................................................................................................................................................... 18
FEATURES OF ANGINA ............................................................................................................................................ 18
MANAGEMENT OF ANGINA .................................................................................................................................... 18
NITRATES ................................................................................................................................................................. 19

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 DEVELOPMENT OF CARDIOVASCULAR SYSTEM 2
CARDIOVASCULAR SYSTEM

MYOCARDITIS.............................................................................................................................................................. 19
SUDDEN CARDIAC DEATH ........................................................................................................................................... 20
VENTRICULAR INFARCT AND HYPERTROPHY .............................................................................................................. 20
MYOCARDIAL INFARCTION ......................................................................................................................................... 20
BLOOD SUPPLY TO HEART ....................................................................................................................................... 20
FEATURES OF MI ..................................................................................................................................................... 21
MORPHOLOGY OF MI.............................................................................................................................................. 22
COMPLICATIONS OF MI .......................................................................................................................................... 23
ENZYMES IN MI ....................................................................................................................................................... 23
DIAGNOSIS IN ISCHEMIC HEART DISEASE ............................................................................................................... 24
MANAGEMENT OF MI ............................................................................................................................................. 25
THROMBOLYSIS ....................................................................................................................................................... 26
WARFARIN .............................................................................................................................................................. 26
AORTIC DISSECTION .................................................................................................................................................... 26
ARRHYTHMIAS ............................................................................................................................................................ 27
CARDIAC CONDUCTION .......................................................................................................................................... 27
GENERAL FEATURES OF ARRHYTHMIA.................................................................................................................... 29
ATRIAL FLUTTER ...................................................................................................................................................... 29
ATRIAL FIBRILLATION .............................................................................................................................................. 29
VENTRICULAR TACHYCARDIA .................................................................................................................................. 30
VENTRICULAR FIBRILLATION ................................................................................................................................... 31
MANAGEMENT OF ARRHYTHMIA ........................................................................................................................... 31
HEART BLOCK .............................................................................................................................................................. 32
VENTRICULAR PREMATURE CONTRACTION ............................................................................................................... 33
TORSADES DE POINTES ............................................................................................................................................... 33
WPW SYNDROME ....................................................................................................................................................... 34
ATHEROSCLEROSIS ...................................................................................................................................................... 34
CAUSES OF ATHEROSCLEROSIS ............................................................................................................................... 34
FEATURES OF ATHEROSCLEROSIS ........................................................................................................................... 35
MORPHOLOGY IN ATHEROSCLEROSIS .................................................................................................................... 35
DIAGNOSIS OF ATHEROSCLEROSIS .......................................................................................................................... 35
HYPOLIPIDEMIC DRUGS .......................................................................................................................................... 36
PREVENTION OF ATHEROSCLEROSIS ....................................................................................................................... 37
CARDIAC TUMOURS .................................................................................................................................................... 37

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 DEVELOPMENT OF CARDIOVASCULAR SYSTEM 3
CARDIOVASCULAR SYSTEM

RHEUMATIC FEVER ..................................................................................................................................................... 38

FEATURES OF RHEUMATIC FEVER ........................................................................................................................... 38
CRITERIA OF RHEUMATIC FEVER............................................................................................................................. 39
MORPHOLOGY OF RHEUMATIC FEVER ................................................................................................................... 39
DIAGNOSIS OF RHEUMATIC FEVER ......................................................................................................................... 40
MANAGEMENT OF RHEUMATIC FEVER .................................................................................................................. 40
CARDIOMYOPATHY ..................................................................................................................................................... 40
FEATURES OF CARDIOMYOPATHY .......................................................................................................................... 40
DILATED CARDIOMYOPATHY .................................................................................................................................. 41
RESTRICTIVE CARDIOMYOPATHY ............................................................................................................................ 41
HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY ................................................................................................ 41
CONGENITAL HEART DISEASE ..................................................................................................................................... 42
FEATURES OF CONGENITAL HEART DISEASE........................................................................................................... 42
TETRALOGY OF FALLOT ........................................................................................................................................... 43
ATRIAL SEPTAL DEFECT ........................................................................................................................................... 44
VENTRICULAR SEPTAL DEFECT ................................................................................................................................ 45
PATENT DUCTUS ARTERIOSUS ................................................................................................................................ 46
TRICUSPID ATRESIA ................................................................................................................................................. 46
COARCTATION OF AORTA ....................................................................................................................................... 47
TOTAL ANOMALOUS PULMONARY VENOUS CONNECTION ................................................................................... 48
TRANSPOSITION OF GREAT VESSELS ....................................................................................................................... 48
EISENMENGER SYNDROME ..................................................................................................................................... 49
HEART FAILURE ........................................................................................................................................................... 49
FEATURES OF HEART FAILURE ................................................................................................................................ 49
DIAGNOSIS OF HEART FAILURE ............................................................................................................................... 50
MANAGEMENT OF HEART FAILURE ........................................................................................................................ 50
CARDIAC GLYCOSIDE ................................................................................................................................................... 51
DIGOXIN .................................................................................................................................................................. 51
DIGITOXIN ............................................................................................................................................................... 52
FEATURES OF DIGITALIS TOXICITY .......................................................................................................................... 52
MANAGEMENT OF DIGITALIS TOXICITY .................................................................................................................. 53
VALVULAR HEART DISEASE ......................................................................................................................................... 53
GENERAL FEATURES OF VALVULAR DISEASES ........................................................................................................ 53
MITRAL STENOSIS ................................................................................................................................................... 53

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 DEVELOPMENT OF CARDIOVASCULAR SYSTEM 4
CARDIOVASCULAR SYSTEM

MITRAL REGURGITATION ........................................................................................................................................ 54

MITRAL VALVE PROLAPSE ....................................................................................................................................... 55
AORTIC STENOSIS .................................................................................................................................................... 55
AORTIC REGURGITATION ........................................................................................................................................ 56
TRICUSPID REGURGITATION ................................................................................................................................... 56
PULMONARY STENOSIS ........................................................................................................................................... 57
ENDOCARDITIS ............................................................................................................................................................ 57
ETIOLOGY OF ENDOCARDITIS ................................................................................................................................. 57
SITE OF ENDOCARDITIS ........................................................................................................................................... 58
FEATURES OF ENDOCARDITIS ................................................................................................................................. 58
MANAGEMENT OF ENDOCARDITIS ......................................................................................................................... 59
PERICARDIAL DISEASES ............................................................................................................................................... 59
GENERAL FEATURES OF PERICARDIUM ................................................................................................................... 59
CARDIAC TAMPONADE ........................................................................................................................................... 59
PERICARDITIS .......................................................................................................................................................... 60
HYPERTENSION ........................................................................................................................................................... 61
BLOOD PRESSURE ................................................................................................................................................... 61
CAUSES OF HYPERTENSION..................................................................................................................................... 62
FEATURES OF HYPERTENSION ................................................................................................................................. 62
RENOVASCULAR HYPERTENSION ............................................................................................................................ 62
MORPHOLOGY OF HYPERTENSION ......................................................................................................................... 63
MANAGEMENT OF HYPERTENSION ........................................................................................................................ 63
VASODILATORS ....................................................................................................................................................... 64
ARTERIOLAR DILATORS ........................................................................................................................................... 64
VENOUS DILATORS .................................................................................................................................................. 64
ACE INHIBITORS ...................................................................................................................................................... 64
ARB .......................................................................................................................................................................... 65
CALCIUM CHANNEL BLOCKER ................................................................................................................................. 65
BETA BLOCKERS....................................................................................................................................................... 66
CLONIDINE .............................................................................................................................................................. 66
METHYLDOPA.......................................................................................................................................................... 67
MANAGEMENT OF HYPERTENSIVE EMERGENCY AND URGENCY ........................................................................... 67

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 DEVELOPMENT OF CARDIOVASCULAR SYSTEM 5
CARDIOVASCULAR SYSTEM

KEY TO THIS DOCUMENT

Text in normal font – Must read point.

Asked in any previous medical entrance
examinations

Text in bold font – Point from Harrison’s

th
text book of internal medicine 18
edition

Text in italic font – Can be read if

you are thorough with above two.

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 DEVELOPMENT OF CARDIOVASCULAR SYSTEM 6
CARDIOVASCULAR SYSTEM

DEVELOPMENT OF CARDIOVASCULAR SYSTEM

First organ formed during embryogenesis Heart

Development of heart 2nd to 8th week
Development of septal defects in fetal heart 5 – 8 weeks
Ectopia cordis associated with Heart
Cardiac jelly is secreted by Myocardium
Cardiac jelly contributes to the formation of Endocardium
Development of heart Dorsal mesocardium forms transverse pericardial sinus,
Myosites arise from splanchnopleuric mesoderm,
Purkinje fibres develop from splanchnopleuric
mesoderm, Neural crest cells have role in development
of muscular and subpulmonary infunbibulum,
Endocaridal cushion develops from cardiac jelly
Development of interatrial septum Perforation in septum primum forms
foramen secundum, foramen secundum
maintains right to left shunt, septum
secundum is situated to the right of
septum primum, septum primum closes at
day 42 of development
Left horn of sinus venosus forms Coronary sinus
Interventricular septum Muscular interventricular septum, conus
septum, AV endocardial cushion
Membranous part of interventricular Anterior part between RV and LV,
septum posterior part between RA and RV
Membranous part of atrioventricular part of RA and LV
interventricular septum is between
Premature closure of foramen ovale results in Right ventricular hypertrophy
Patent foramen ovale is due to failure of fusion of Septum primum and septum secondum
Aneurysm of sinus of valsalva usually arise from Right aortic sinus
Muscular component of dorsal aorta develops from Paraxial mesoderm
Axial artery of Upper Limb is derived from Seventh Intersegmental artery
Most important structure involved in development of Supracardinal vein and subcardinal vein
inferior vena cava
Vitelline vein forms Hepatic vein, Inferior mesenteric vein, inferior vena
cava
Does NOT derive from vitelline vein Superior vena cava
Left sided superior vena cava drains into Coronary sinus
Kommerell’s diverticulum Anatomical remnant of right aortic arch
Smooth portion of right atrium is derived Sinus venosus
from

ANATOMY OF CARDIOVASCULAR SYSTEM

Thinnest portion of Myocardial wall Right atrium and Left atrium

Sinoatrial node is situated at Junction of SVC and Right atrium
AV node lies at Interatrial septum

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 PHYSIOLOGY OF CARDIOVASCULAR SYSTEM 7
CARDIOVASCULAR SYSTEM

Fibres of AV junction Modified Nerve fibres

Ventricular muscle receives direct innervation from Purkinje fibres
Triangle of Koch Coronary sinus opening, Tendon of todaro, Septal
leaflet of tricuspid valve
Boundary of Koch triangle NOT formed by Limbus fossa ovalis
NOT a boundary of Koch’s triangle Origin of Left Coronary artery
Feature of right atrium Coronary sinus lies between fossa ovalis and IVC
Structures associated with internal Sinus of keith, triangle of Koch, tendon of
surface of right atrium todaro, Waterson groove
NOT a part of interior of Right atrium Trabeculae carnea
Coronary sulcus Between right atrium and aorta. Right
coronary artery passes through it.
Anatomy of right ventricle Most prominent trabeculation, Crista supraventricularis
separate tricuspid valve and pulmonary valve, Apex
trabeculated, TV and PV share fibrous continuity
Right ventricle Conus, outflow tract
Annulus of Vieussen around Right ventricular outflow tract
Base of heart is related to Descending aorta
Area of mitral orifice in adults 4-6 cm^2
Central fibrous body of heart formed by Right fibrous trigone with membranous
part of ventricular septum
Commonest variation in arteries arising from arch of Left common carotid artery arising from
aorta brachiocephalic trunk
Sympathetic supply to heart T1 to T5
In angina pectoris, pain radiating down the left arm is Thoracic splanchnic nerve
mediated by increased activity in afferent (sensory)
fibres contained in
Buffer nerve Carotid sinus nerve and vagal fibres from
aortic arch
Superficial cardiac plexus Below aortic arch
Left coronary plexus Deep cardiac plexus
Right coronary plexus Both superficial and deep cardiac plexus

PHYSIOLOGY OF CARDIOVASCULAR SYSTEM

GENERAL FEATURES OF PHYSIOLOGY OF CARDIOVASCULAR SYSTEM

Duration of Cardiac cycle in man 0.8 seconds

During cardiac cycle Mitral and aortic valve never open at
same time
Left ventricular systole corresponds to Auricular diastole
Minimum motion of heart during cardiac imaging Mid diastole
LEAST correct statement During exercise systole is shortened more than diastole
Heart stops in Diastole in Hyperkalemia
AV valves open at the beginning of Diastole
Isometric relaxation of cardiac cycle ends with Opening of AV valve
At the end of isometric relaxation phase AV valves open

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 PHYSIOLOGY OF CARDIOVASCULAR SYSTEM 8
CARDIOVASCULAR SYSTEM

Closure of aortic valve corresponds to beginning of Isovolumetric relaxation

Isovolumetric dilatation of ventricles is at Closing of Semilunar valves
Aortic valve closes at the end of Protodiastole
During cardiac cycle, opening of aortic valve takes place End of isovolumetric contraction
at
Maximum pressure rise in ventricles Isovolumetric contraction
during
Phase of cardiac cycle follows immediately Isovolumetric contraction
after beginning of QRS wave
Isovolumetric relaxation precedes Ventricular ejection
Initiation of opening of aortic valve occurs when Ventricular pressure is more than aortic pressure
Correlate with isovolumetric contraction Both valves are open
Preload is associated with Isotonic contraction with shortening of
muscle fiber
Volume determining preload End diastolic volume of ventricles
End diastolic ventricular volume 130 ml
End diastolic volume increases in Decreasing venous compliance
Intrinsic heart rate is determined by IV administration of atropine, atenolol
Cardiac output in L/min divided by heart rate equals Mean stroke volume
Cardiac output in an adult is nearly 5 litres
Percentage of Cardiac output concentrated by Renal 25%
blood flow
Maximum cardiac output during pregnancy 32 weeks
Cardiac output is decreased in Rapid arrhythmia
Low cardiac output is associated with Arrhythmia
Cardiac output decreases during Standing from lying position
Cardiac output can be determined by Fick’s principle, ECHO, Thermodilution
Direct fick method for estimation of cardiac output O2 content of arterial blood, O2 consumption per unit
requires time, O2 content of blood from right ventricle
Fick’s law Passive osmosis along concentration gradient only
Scientific principle for the basis for thermodilution Stewart Hamilton priniciple
method used in measurement of cardiac output by
pulmonary catheter
Most recent advance in non invasive cardiac output Electrical impedance cardiography technology
monitoring
Cardiac index cardiac output/body surface area
Cardiac index in normal person 3.2 (2.6 – 4.2)
Cardiac index of normal person 3.2 l/min/m^2
Cardiac output in L/min divided by heart rate equals Mean stroke volume
Preload to heart depends upon Stroke Volume
Stroke volume is decreased by Increasing heart rate
Stroke volume is decreased in Arrhythmia
Gorlin formula Area of flow across valve
Hakki formula Aortic valve area
Severity of shunt Pulmonary blood flow/systemic blood flow (Qp/Qs)
Venous return (mean systemic filling pressure – right atrial
pressure)/resistance to venous return
Venous return to heart from lower limb is NOT affected Arterial pressure
by
Venous return to heart during quiet standing facilitated Calf muscle contraction during standing, valves in

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 PHYSIOLOGY OF CARDIOVASCULAR SYSTEM 9
CARDIOVASCULAR SYSTEM

by perforators, sleeves of deep fascia

When a person changes from standing to lying down Venous return to heart rises immediately
position
Supine to upright position Decrease in central venous pressure, Rise in heart rate,
Decrease in cardiac output, Decrease in stroke volume
Shift from supine to upright NOT occur Rise in central venous pressure
Coronary blood flow Directly related to perfusion pressure and inversely
related to resistance
Amount of coronary blood flow 250 ml/min
Coronary blood flow in left coronary artery is maximum Ventricular diastole
during
Coronary blood flow stops during Isometric contraction
Blood pressure during exercise is increased in Coronary circulation
Reflex noradrenergic discharge during fall in blood Coronary circulation
pressure causes vasodilatation in
Most important metabolic factor affecting coronary Hypoxia
blood flow
Cardiac oxygen demand Has a constant relation to external work done by heart
Myocardial oxygen demand Correlates with heart rate, Constant relation to external
cardiac work, Depends of preload, afterload,
intramyocardial tension, myocardial muscle mass
Myocardial oxygen consumption Directly proportional to mean arterial pressure
Myocardial oxygen demand correlate with Heart rate
Oxygen utilization by ventricular muscles at rest 10 ml/100 gm/ min
Negative G Cardiac output increases, Cerebral artery pressure
increases, Blood centrifuged towards head, Red out
Aviator subjected to negative G Cerebral arterial pressure rises
Baroreceptor Nucleus tractus solitarius
Baroreceptors are mostly sensitive to Systolic blood pressure
Discharge from baroreceptors causes inhibition of Rostral ventrolateral medulla
Baroreceptor stimulation produce Decreased heart rate and BP, Decreased cardiac
contractility
Ligature tied proximal to baroreceptors (below carotid Hypertension and tachycardia
sinus)
Means of studying acute physiological Sinoaortic denervation (lowers body
response to arterial baroreceptor negative pressure)
unloading
Vasomotor centre of medulla Acts along with cardiovagal centre to maintain blood
pressure
Inhibition of Vasomotor centre causes Decrease in BP
Pressure on carotid sinus cause Reflex bradycardia
On cutting or severing sinus nerve in dog, cause Increase in mean blood pressure
Clamping of carotid arteries below (proximal) carotid Increase in blood pressure and increase in heart rate
sinus likely to produce (stimulates vasomotor center – sympathetic response)
Effect of bilateral Carotid compression above Carotid Stimulates vagal parasympathetic center
Sinus
Single most important factor in control of autonomic Sympathetic stimulation
contractility of heart
Features of sympathetic stimulation of heart Increased contractility, increased heart rate, increased
conduction velocity
Sympathetic stimulation Increased HR, BP, total peripheral resistance, Decreased

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 PHYSIOLOGY OF CARDIOVASCULAR SYSTEM 10
CARDIOVASCULAR SYSTEM

venous capacitance
Sympathetic stimulation does NOT cause Increase in venous capacitance
cAMP specific phosphodiesterase inhibitor Increases contractility
on contractility of isolated strips of rabbit
heart
Human heart Heart rate increases with parasympathetic denervation
Features suggesting denervation Unregulated firing of individual muscle fibres, presence
of positive sharp waves, spontaneous firing of motor
units
Denervated heart has More heart rate
In a patient with transplanted heart, reason for Epinephrine from medulla
increased cardiac output during exercise
Plateau phase of myocardial action potential is due to Influx of Ca++
Factors increasing length of ventricular cardiac muscle Increased venous tone, Increased total blood volume,
fibres Increased negative intrathoracic pressure
Left ventricle performs more than right due to Arterial pressure
difference in
Ejection fraction (left ventricle) Stroke volume/end diastolic volume
Normal left ventricular ejection fraction 65%
Pressure in right atrium Less than 6 mm Hg
Right Ventricular Systolic Pressure 25 mm Hg
Right ventricular diastolic pressure 0 – 12 mm Hg
A 0.5 litre blood loss in 30 minutes will lead to Slight increase in heart rate and normal BP
A patient with increased BP and decreased heart rate is Increased ICT, Brain tumor, Head trauma
likely to have
Bradycardia can occur in Myxoedema, during convalescence, complete heart
block
Drug linked with increased cardiac mortality Rofecoxib
When blood flow stops the pressure is given by Mean Circulatory filling pressure
Main site of Peripheral vascular resistance Precapillary arterioles
Splanchnic circulation 25-30% of total circulation
Shape of arterial pulse is influenced by Arterial wall expansion

OXYGEN CONSUMPTION

Whole body 250 ml/min

Liver 51 ml/min
Skeletal muscle 50 ml/min
Brain 49 ml/min
Rest of muscle 44 ml/min
Heart muscle 29 ml/min
Kidney 18 ml/min
Skin 12 ml/min

MEAN ARTERIAL PRESSURE

Mean arterial pressure Diastolic + one third of pulse pressure

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CARDIOVASCULAR SYSTEM

Peripheral resistance Mean arterial pressure as it remains constant

Mean arterial pressure (SBP + 2DBP)/3

PULSE PRESSURE

Pulse pressure lowest in arterial system in Capillaries

Pulse pressure Systolic pressure - diastolic pressure
Pulse pressure is increased by Decrease in arterial compliance
Varying pulse pressure with Normal rhythm Left ventricular failure
Wide pulse pressure NOT seen in Congestive heart failure

VASCULAR SYSTEM

Circulation Pulsatile flow affects gene transcription, Increased

viscosity increases mean blood pressure, Hematocrit
does NOT markedly change peripheral resistance,
Pulsatile flow is recommended
Marey’s law is Relationship with heart rate and blood pressure
Law relating distending pressure and tension in a vessel Law of Laplace
wall
Law related to wall tension Laplace law
Laplace law for a cylinder P = T/r
Laplace law has NO role in Liver
50% reduction in arterial diameter causes Reduction in flow 16 times
Velocity of blood in aorta 22 cm/sec
Velocity of blood is inversely proportional to Cross sectional area
Reservoirs of blood in cardiovascular Venules
system
Velocity of blood is maximum in Large veins
Flow is laminar in small vessels because Effective velocity in small vessels is less
Which increase turbulence in blood flow Increase diameter of blood vessel
Blood flow Liver > kidney > brain > heart
Local control of blood flow NOT seen in Skin
Which is NOT increased during exercise Peripheral Vascular resistance
Storage pool of blood Vein
Blood supply in splanchnic vessels decrease due to Venoconstriction with decreased blood flow
In a younger subject whose aorta has high elastin Diastolic pressure is maintained, pulse pressure is
content narrow
Maximum difference of BP occurs between Femoral artery and femoral vein
Classical finding in AV fistula Sinus tachycardia
Capillaries Greatest cross sectional area, Contains 5% blood,
Contains less blood than veins, Have single layer of cells
bounding the lumen, Site of gaseous exchange, Lined by
endothelium
Capillaries Larger quantity of blood than veins, site of gaseous
exchange, lined by endothelium
Capillaries Greatest cross sectional area, less blood than veins,

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 SYNCOPE 12
CARDIOVASCULAR SYSTEM

single layer of cells

Changes in blood passing through systemic capillaries Hematocrit increase, pH decrease, increase in protein
content, shift of O2 dissociation curve to right
Pre capillary sphincter relaxation mediated by Local hormones
Common structural feature seen in all capillaries is Continuous basement membrane
Pericytes Wrap around capillaries
At a constant blood flow, an increase in Greater surface for diffusion of molecules
number of perfused capillaries improves
the exchange between blood and tissue
because of
Distribution of blood flow is mainly regulated by Arterioles
Maximum peripheral vascular resistance Arterioles
Regulation of blood flow is maintained by Arterioles
Cutaneous shunt vessels Role in thermoregulation
Quantitatively most important means of Decreasing local vascular resistance
increasing flow to an actively
metabolizing tissue

SYNCOPE

NOT a situational syncope Deglutition syncope, Cough syncope, Micturition

syncope
Mess trick and fainting lark is associated with Syncope
Head up tilting for diagnosing Syncope
Least useful investigation in neurocardiogenic syncope Carotid duplex scan
Drug of choice in carotid sinus syncope Ephedrine
Biofeedback therapy is not applicable for Vasovagal syncope

HEART SOUNDS

FIRST HEART SOUND

First heart sound occur during the period of Isovolumetric contraction

First heart sound Lower frequency than S2, Caused by closure of mitral
valve, Better heard with diaphragm of stethoscope
Soft S1 MR, VSD, calcified valve, long standing severe MS,
pleural effusion, obesity
Loud S1 Short PR interval, Tachycardia
Loud S1 in mitral stenosis is caused by Prolonged flow through mitral valve
Reversed splitting of S1 LBBB, atrial myxoma

SECOND HEART SOUND

Incisura of arterial pulse corresponds to Second heart sound

Aortic component of Second heart sound is best heard Ludwig’s angle to right

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 HEART SOUNDs 13
CARDIOVASCULAR SYSTEM

at
Heart sounds occurring shortly after S2 Opening snap, pericardial knock, tumour plop
Heart sound NOT occurring shortly after S2 Ejection click
Tumor plop Low pitched
Single S2 TOF, pulmonary atresia, severe pulmonary stenosis
Loud pulmonary component of S2 Pulmonary hypertension, Eisenmenger syndrome
Pulmonary component of second heart sound is soft Fallot’s tetrology
and inaudible on auscultation
Hang out time is related to Splitting of second heart sound
Wide split S2 ASD, MR, pulmonary stenosis
Fixed(wide) splitting of S2 ASD, Pulmonary stenosis, pulmonary embolism
Wide fixed split S2 with ejection systolic murmur in left Ostium primum atrial septal defect
second intercostals space, left axis deviation
Reversed splitting of S2 Aortic stenosis, Left bundle branch block, systemic
hypertension, PDA, post stenotic dilatation in AS
Severe Paradoxical S2 split AS

THIRD HEART SOUND

Loud S3 Severe MR
Third heart sound Constrictive pericarditis, ASD, VSD, athletes, LVF
Third heart sound is due to Ventricular filling NOT at the time of atrial systole
S3 heard over Left ventricle
S3 not heard in Severe MS

FOURTH HEART SOUND

Fourth heart sound is due to Ventricular filling

S4 IHD, long standing hypertension, hypertrophic
cardiomyopathy, abnormal forceful left ventricular
dilatation, Aortic stenosis, Hypertension
S4 Aortic stenosis, Hypertension, HOCM
S4 Thyrotoxicosis, acute MI
Fourth heart sound Heard during ventricular filling phase
S4 is NOT heard in Ventricular aneurysm

SNAP, CLICK AND THRILL

Opening Snap High pitched, Early diastolic

Opening snap in mitral area corresponds to Dicrotic notch of carotid pulse
Dicrotic notch in arterial pulse is due to Closure of aortic valve
NOT a diastolic sound Ejection click
Systolic thrill in second and third intercostal space Subpulmonic VSD, pulmonic stenosis, Ebstein anomaly
Double apical impulse Aortic stenosis, HOCM

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 ARTERIAL PULSE AND JUGULAR VENOUS PULSE 14
CARDIOVASCULAR SYSTEM

MURMUR

Still murmur In normal children and adolescents

Right sided murmur Usually increase with inspiration except pulmonary ejection
sound
Valsalva maneuver phase I Forced expiration against closed glottis, increased BP and
decreased heart rate
Phase of valsalva maneuver in which Phase I
heart rate decrease
Valsalva maneuver Decreases length and intensity except HOCM, MVP
Standing Diminishes murmur except HOCM, MVP
Hand grip increases MS, PS, MR, AR, VSD
Continuous murmur AV communication, Aortic sinus of Valsalva rupture,
Coarctation of aorta
Continuous murmur PDA, shunt between pulmonary and subclavian artery
Continuous murmur NOT seen in VSD with aortic regurgitation
Continuous murmur NOT seen in Mitral stenosis with mitral regurgitation, peripheral
pulmonary stenosis, VSD with AR
An early systolic murmur may be caused by Small ventricular septal defect, papillary muscle
dysfunction, Tricuspid regurgitation
MC cause of midsystolic murmur in adult Aortic stenosis
Pansystolic murmur MR, VSD, TR
To and fro murmur VSD with AR, AR with MR, Repaired
TOF
Murmur heard in utero Gerbode effect (LV to RA shunt)
New systolic murmur after MI Rupture of interventricular septum, papillary muscle
dysfunction, ischemic cardiomyopathy
Intensity of systolic murmur increased in Severe AS
Carey comb murmur Delayed diastolic murmur, rheumatic fever, low pitched
murmur
Cole cecil murmur AR murmur in mid axillary area
Gibson murmur Machinery murmur in PDA
Graham Steel murmur Pulmonary regurgitation, pulmonary arterial hypertension
Seagull murmur Ruptured chorda tendinae
Means Lerman scratch Uncommon cardiac murmur in hyperthyroidism, may mimic
pericardial rub
Best position for examining cardiac murmurs in child Recumbent
Abnormal change in pregnancy Diastolic murmur
Investigation for diastolic murmur Echocardiography

ARTERIAL PULSE AND JUGULAR VENOUS PULSE

GENERAL FEATURES OF PULSE

Asymmetric pulse Dissection of aorta, Aortoaortitis, Aneurysm of

descending aorta
Pulsus parvus et tardus Weak and delayed pulse, seen in aortic stenosis

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 ARTERIAL PULSE AND JUGULAR VENOUS PULSE 15
CARDIOVASCULAR SYSTEM

PULSUS BISFERIENS

Pulsus bisferiens Two systolic peaks

Dicrotic pulse Two peaks one in systole and other in
diastole
Pulsus bisferiens AR, AR+AS, Hypertrophic cardiomyopathy
Pericardial tamponade is NOT associated with Pulsus bisferiens
Pulsus bisferiens best felt in Radial artery

PULSUS PARADOXUS

Pulsus paradoxus is defined as Marked and exaggerated inspiratory fall

in systolic BP in which the Korotkoff’s
sound disappears during inspiration
Pulsus paradoxus Cardiac tamponade
Pulsus paradoxus is seen in Constrictive pericarditis, Cardiac tamponade, Massive
pulmonary embolism, COPD, severe asthma,
emphysema, hypovolemic shock
Pulsus paradoxus is NOT seen in Hypertension, MI
Pulsus paradoxus is NOT seen in Aortic regurgitation

PULSUS ALTERANS

Pulsus alterans Left ventricular failure

Pulsus alterans Ischemic heart disease

JUGULAR VENOUS PULSE

JVP a-x descent atrial relaxation, v-y emptying of blood from

right atrium into right ventricle, y-a ascent filling of right
atrium from vena cava
JVP finding in cardiac tamponade Prominent x descent, Absent y descent
Typical JVP finding in cardiac tamponade Absent y descent
Paradoxical Inspiratory rise in JVP Constrictive Pericarditis, Kussmaul sign
Square root sign in JVP Constrictive pericarditis
JVP is NOT raised in Hypovolemic shock
Should NOT rise in pregnancy JVP
Cannon wave Complete heart block
Giant ‘a’ wave is seen in Tricuspid stenosis, right heart failure, pulmonary
hypertension
A wave is exaggerated in Tricuspid stenosis, Complete heart block, junctional
rhythm, pulmonary hypertension
A waves in JVP are absent in Atrial fibrillation
C wave in JVP Ventricular contraction
C wave in JVP is due to Bulging of tricuspid valve into right atrium

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 ELECTROCARDIOGRAM 16
CARDIOVASCULAR SYSTEM

c-wave in JVP due to Isometric Contraction (Bulging of tricuspid)

C wave in JVP Bulging of tricuspid into right atrium
v-wave in JVP Filling of Right Atrium due to venous return
V wave in JVP is due to Atrial filling while TV closed

ELECTROCARDIOGRAM

GENERAL FEATURES OF ECG

Sum of voltage of 3 leads in ECG 5 millivolts Increased cardiac muscle mass

Depolarization of atria in ECG is seen in P wave
Depolarization in ECG by P and QRS complex
P wave size in right atrial enlargement 2.5 mm
Ventricular Depolarization starts from Left part of Interventricular septum
Time required for ventricular depolarization 0.08 to 0.1 sec
QRS complex indicates Ventricular depolarization
QRS duration 100 - 120 ms Normal, Left anterior fascicular block, left posterior
fascicular block, Incomplete RBB
Wide QRS complex > 120 ms Hyperkalemia, WPW syndrome, Ventricular tachycardia
Wide QRS complex typically seen in Bundle branch block
Massive QRS is associated with Pompe’s disease
Athletic syndrome characterized by Increased amplitude of QRS complex
Low QRS voltage Pericardial effusion
Low QRS voltage with left ventricular hypertrophy Cardiac amyloidosis
Component of ECG varying with heart QT interval
rate
Ventricular contraction Beginning of Q wave to end of T wave, Beginning of R
wave to end of T wave, if Q wave is absent
SNHL, Syncope, Prolonged QT interval Jervell Lange Neilson Syndrome
Vagal stimulation of heart causes Increased RR interval in ECG
Repolarization of ventricles is indicated T wave
by
QRS and ST junction J point
Plateau phase corresponds with ST segment
Brugada syndrome Normal structure of heart with ST elevation in V1, V2 and V3
Brugada syndrome is due to mutation of Cardiac sodium channel SCN5A
Treatment of Brugada syndrome Quinidine, Isoprotenol
J wave (Osborn wave) Hypothermia
Normal axis of ECG in adult male -30 to +110 *
Left axis deviation is seen as Positive in lead I and negative in lead II
Instantaneous mean vector Equal and same as mean QRS vector, It is drawn
through centre of vector in a direction from base
towards apex, Summated vector of generated potential
at particular instant cause by inflowing septal
depolarization, When a vector is exactly horizontal and
directed toward the person’s left side, vector is said to
extend in direction of 0*

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 ELECTROCARDIOGRAM 17
CARDIOVASCULAR SYSTEM

Electromechanical systole Between Q and S2

If carotid transducer is NOT functioning we can NOT LVET and PEP
obtain
PEP/LVET ratio is increased in Left ventricular systolic failure, aortic
stenosis, left bundle branch block
NOT measured without carotid transducer LVET, PEP

ECG FEATURES OF HYPERKALEMIA

Hyperkalemia Peaked T waves, loss of P waves, sine waves

Prolonged PR interval, prolonged QRS interval,
ventricular asystole
ECG changes in hyperkalemia Wide QRS, Tall T waves, Prolonged PR interval, Sine
wave pattern, disappearance of P waves
Tall T waves Hyperkalemia
NOT an ECG feature of hyperkalemia Prolonged QT interval
NOT true about hyperkalemia U wave
Calcium is indicated in Hyperkalemia
NOT a treatment of hyperkalemia without ECG changes Calcium gluconate

ECG FEATURES OF HYPOKALEMIA

Hypokalemia ECG U wave, ST depression, flattened or inverted T wave,

prolonged PR interval
ECG with ST segment of prolongation and late T wave Hypokalemia
ECG finding in hypokalemia Increased PR interval with ST depression

ECG FEATURES OF HYPERCALCEMIA

Narrowed QT interval, polyuria, polydipia, nausea, Hypercalcemia

altered sensorium for last 2 days. squamous cell
carcinoma
QT interval shortened in Hypercalcemia

ECG FEATURES OF HYPOCALCEMIA

ECG feature of Hypocalcemia Prolonged QT interval

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CARDIOVASCULAR SYSTEM

ANGINA

FEATURES OF ANGINA

Critical narrowing of coronary vessel to More than 70%

cause angina
Most important factor in causation of cardiac arrest Anoxia
Tietze syndrome usually Second costal cartilage
Angina pectoris carried by Middle and inferior cervical cardiac nerve
Potassium channel opener with anti anginal activity Nicorandil
Potassium channel opener Penicidin
Hypertensive developed angina Propanolol
Ranolazine Piperazine derived antianginal agent, may be used as
first line agent in chronic angina, may improve glycemic
control
Drugs that can worsen angina Dipyridamole, Thyroxine, Sumatriptan
Does NOT worsen angina Oxephedrine
Stable angina is associated with Physical exertion
Cardiac markers in stable angina Unchanged
Unstable angina are true Recent angina, ST elevation or depression, rest pain
Drug used in Unstable Angina Eptifibatide
Drug for Variant angina/Unstable angina/Prinzmetal Diltiazem
angina
Drug of choice for variant angina Nitrates
Propanolol is NOT indicated in Variant angina
Prinzmetal angina Transient ST elevation
Prinzmetal angina Pain at rest, transmural ischemia, ST elevation during
attack, ST depression with pain
MC site of focal spasm in Prinzmetal angina Right coronary artery
Drug increasing severity of prinzmetal angina Aspirin

MANAGEMENT OF ANGINA

Ranolazine pFOX inhibitor

Ranolazine is a selective inhibitor of iNa current
Ranolazine is metabolized primarily by CYP3A4
Unique feature of ranolazine Anti ischemic effects are achieved without
clinically meaningful change in heart rate
and blood pressure
Ranolazine NO effect of BLOOD PRESSURE, Not indicated in acute
angina, Improves glycemic control
Dipyridamole Adenosine uptake inhibition
Beneficial effect of metoprolol in Increase in diastolic filling time
management of secondary angina

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CARDIOVASCULAR SYSTEM

NITRATES

Drugs decreasing preload Glyceryl trinitrate, ACE inhibitors, Sodium nitroprusside

Nitrates Release NO, cause vasodilatation, high first pass
metabolism
Nitrates Decreases left ventricular end diastolic pressure, Direct
reduction of oxygen consumption of myocardial cell,
Dilatation of capacitance vessels, Decreasing size of
heart
Anti anginal action of nitrates Decrease myocardial O2 consumption, decrease both
pre and after load, cause favourable redistribution of
coronary blood flow
GTN given by sublingual route because of Hepatic first pass metabolism
Nitrates metabolized by Guanathione reductase
Nitrates does NOT cause Increase in cardiac work
Nitrates NOT used in Renal colic
Nitrate does NOT undergo first pass metabolism Isosorbide mononitrate
NOT given by sublingual route Isosorbide 5 mononitrate
Longest acting nitroglycerine preparation Pentaerythritol tetranitrate
Nitrate associated with allergic reaction Pentaerythritol tetranitrate
Nitrate bypassing cysteine dependent Molsidomine
pathway
Route of amyl nitrite Inhalation
Nitroglycerin cause Hypotension and TACHYCARDIA
Side effects of nitroglycerine Hypotension, Tachycardia, Methemoglobinemia,
Vasodilatation
Treatment of idiosyncratic effects of Atropine
nitrates

MYOCARDITIS

Heart muscle Act as syncitium, Single nuclei, Gap junctions, Has

branching
Cardiac muscle is able to function as syncitium because Gap junction
of structural presence of
Intercalated discs present in Cardiac muscle
Myocarditis may be associated with Trichinosis, Corynebacterium diphtheria, SLE
Myocarditis can be associated with SLE, radiation
Infantile myocarditis and pericarditis is due to Coxsackie B
MC non infective myocarditis Granulomatous myocarditis
Giant cell myocarditis Rapidly progressing heart failure, may be
associated with thyroiditis,
tachyarrhythmia are common, steroids
are used in treatment

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CARDIOVASCULAR SYSTEM

SUDDEN CARDIAC DEATH

Cut off for sudden cardiac death 1 hour or less

System most commonly involved in sudden death CVS
Sudden cardiac death may occur in Dilated cardiomyopathy, Hypertrophic cardiomyopathy,
Eisenmenger syndrome
MC ECG abnormality in sudden death Prolonged QT interval

VENTRICULAR INFARCT AND HYPERTROPHY

Factors increasing length of ventricular cardiac muscle Increased venous tone, increased total blood volume,
increased negative intrathoracic pressure
Right ventricular infarct Nocturia, hepatomegaly, ascites
NOT true about right ventricular infarct Normal JVP
Left ventricular hypertrophy is caused by MR,AS,MR
Left ventricular hypertrophy NOT seen in MS
NOT a sign of RVH Lower sternal dullness
NOT true about subendocardial hemorrhage Involves RV wall
Left ventricular function in ventriculography is Technetium
evaluated by
Most accurate investigation for assessing ventricular Echocardiography
function
Cardiotoxicity caused by radiotherapy and Endomyocardial biopsy
chemotherapy is best detected by
Drug of choice in asymptomatic left ventricular Enalapril
dysfunction

MYOCARDIAL INFARCTION

BLOOD SUPPLY TO HEART

Coronary artery Right coronary artery lies in right anterior coronary

sulcus, Left anterior descending artery is a branch of left
coronary artery, SINGLE obtuse marginal artery arise
from left coronary artery, In 85% cases posterior
descending interventricular artery arise from right
coronary artery
Vasodilatation associated with hypotension in Coronary circulation
Right coronary artery lies in Right anterior coronary sulcus
Right coronary artery Diameter less than LCA, RCA arises from anterior aortic
sinus, RCA gives rise to circumflex coronary branch
Branch of right coronary artery Acute marginal, Posterior interventricular
SA node is predominantly supplied by Right Coronary artery
Right coronary artery supplies SA node, AV node, AV bundle
Branches of right coronary artery Acute marginal artery, Posterior interventricular artery,
Posterior ventricular

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 MYOCARDIAL INFARCTION 21
CARDIOVASCULAR SYSTEM

In 85% of patients posterior descending interventricular Right coronary artery

artery arise from
Right coronary artery does NOT supply Right bundle branch
Occlusion of anterior descending branch of LAD will Anterior wall of left ventricle
lead to infection of
Greater volume of myocardial tissue supplied by Left Coronary artery
If circumflex artery gives of the posterior Left dominance
interventricular artery, then arterial supply is called
Left coronary artery Anterior Descending, Circumflex
Widow’s artery Left anterior Descending
Involvement of anterior descending branch of left Anterolateral wall
coronary artery
Anterior wall of left ventricle is supplied Proximal part of left anterior descending
by
Right bundle branch and left bundle Left coronary artery
branch are supplied by
Third coronary artery Conus artery (arteria coni arteriosi from
anterior aortic sinus)
Kugel artery Arteria anastomotica auricularia magna
Common site of occlusion of thrombus Anterior interventricular, Posterior interventricular,
Circumflex
NOT a common site of occlusion of thrombus Marginal artery
Attachment of Thrombus Firm
Left Common cardinal vein forms Oblique vein of Left Atrium
Valveless tributary of coronary sinus Oblique vein of left atrium
Vein in cardiac anterior Interventricular groove Great cardiac vein
Anterior cardiac vein drains into Right atrium
Middle cardiac vein is located in Posterior interventricular sulcus
Coronary sinus Remnant of left horn of sinus venosus, Great middle
and small cardiac vein drain into it, Thebesian valve
guard its opening
Thebesian veins Venae cordi minimi (smallest cardiac veins), open
directly into all four chambers
Coronary sinus ends in Right atrium
Vein NOT draining into Coronary sinus Anterior Cardiac vein
Anterior cardiac vein drains in to Right atrium
Thebesian valve is located in Coronary sinus

FEATURES OF MI

Strongly associated with coronary heart disease Apolipoproteins

Killik classification Myocardial infarction
Shoulder hand syndrome MI
Levine sign Substernal discomfort
Most susceptible to ischemia Myocytes
MC cause of acute epigastric pain Myocardial infarction
Pain is not uniformly present in ST elevation MI
MC artery involved in Myocardial infarction Left anterior descending artery

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 MYOCARDIAL INFARCTION 22
CARDIOVASCULAR SYSTEM

Involvement of anterior descending branch of left Anterolateral wall infarct

coronary artery
Occlusion of anterior descending branch of LAD will Anterior wall of left ventricle
lead to infarction of
MC site of MI Anterior wall of left ventricle
Universal definition of myocardial infarction Sudden unexpected cardiac death with symptoms of
ischemia, Elevation of cardiac biomarkers with new
regional wall motion abnormality, Three times increase
in troponin levels after PCI
Right ventricular infarction Associated with inferior wall MI, JVP is raised, diagnosis
is confirmed by right side chest leads on ECG,
arrhythmia, cardiomegaly, hypotension
Subendocardial infarction Multifocal in nature, often result from hypotension or
shock, epicarditis is NOT seen , does NOT result in
aneurysm
Neonate has recurrent attacks of abdominal pain, Anomalous coronary artery
restless irritability and diaphoresis on feeding. Cardiac
auscultation reveals a non specific murmur. believed to
be at risk of MI
Acute MI associated with Chest pain, Gallop, Systolic murmur in mitral area
Acute coronary syndrome does NOT include Prinzmetal angina
Pain of Myocardial infarction does NOT radiate to Left iliac fossa
Rapid x descent rare in RVMI
MC cause of death immediately after MI Arrhythmia
NOT true about coronary heart disease in india CHD presents a decade later than in western countries
NOT true about coronary heart disease Influence of smoking is only additive to other risk
factors for CHD
Best predictor for coronary heart disease LDL
Used to perform stress echo Dobutamine
Somatotrophin is contraindicated in Ischemic heart disease

MORPHOLOGY OF MI

Major histological feature of MI Coagulative necrosis

Autopsy finding after 12 hours in case of death due to Coagulative necrosis
MI is
Pathology of myocardial infarction Neutrophilic infiltration around coagulative necrosis
Earliest light microscopic change in myocardial Waviness of fibres
infarction (1 – 3 hours)
2 – 3 hours Staining defect
4 – 12 hours Coagulation necrosis
12 – 24 hours Dark mottling
18 – 24 hours Pyknosis
60 year male, acute chest pain, new Q wave, ST Necrotic myofibres with presence of neutrophils
segment depression, succumbed to his illness within 24
hours of admission. Heart revealed presence of
transmural hemorrhagic area over septum and anterior
wall of left ventricle. light microscopy finding
Coagulative necrosis with neutrophilic infiltration in 1-3 days

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 MYOCARDIAL INFARCTION 23
CARDIOVASCULAR SYSTEM

Myocardial infarction seen after

24 – 72 hours Neutrophils and loss of nuclei
Cells seen after 72 hours in infracted area in MI Macrophages
In myocardial infarction, infarct acquires hyperaemic 3 – 7 days
rim with a yellow centre
Myocardial infarct showing granulation tissue has most Within one week
likely occurred
3 – 7 days Macrophages
Granulation tissue following MI 7 – 10 days
A myocardial infarction showing early granulation tissue Within 1 month
has most likely occurred
10 – 12 days Fibrovascular response
7 weeks Fibrosis
Infracted myocardium completely replaced by scar 8 weeks
tissue by
Myocardial scarring completes by 3 months

COMPLICATIONS OF MI

Patient with acute anterior wall MI and hypotension, Angiography and pulmonary angioplasty
immediate treatment
Best modality of treatment in acute inferior wall MI IV fluids
Most deaths in MI occur during First 24 hours
st
Most of deaths in MI 1 day
Reason for shock in inferior wall MI Right ventricular infarction
Parasympathetic activity is associated Inferior wall MI
with
Pansystolic murmur after MI is due to Elevated LA pressure which in turn leads
to rupture of papillary muscle
70 year old, hypertensive male, transmural External cardiac rupture
th
anterolateral MI, stable till 5 day. Painful friction rub
and pleuritic chest pain, persisted despite narcotic and
steroid therapy. On seventh day morning, marked
hypotension. marked distension of jugular veins,
electromechanical dissociation
Post MI Rupture, Leakage at Site of Vascular Anastomosis
Complication of MI occurring between 3 – 7 days Rupture of left venticular free wall
Dressler syndrome Occurs 1 to 4 weeks after myocardial injury, Chest pain
is common, Recurrence may be seen, Responds well to
salicylates
Dressler syndrome is associated with Pleural effusion
Dressler syndrome is Autoimmune
NOT true about Dressler syndrome Myocarditis

ENZYMES IN MI

Correct sequence of increase in enzymes in myocardial CPK, AST, LDH

infarction

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CARDIOVASCULAR SYSTEM

Both CKD and LDH are raised in Myocardial infarction

Increased CK and SGOT levels are seen in Myocardial infarction
NOT a marker of MI Calmodulin
Flipped pattern of LDH isoenzymes Myocardial Infarction
Isoenzyme specific for MI LDH 1
Serum total LDH raised in Muscle crush injury, myocardial infarction, hemolysis
First marker in MI Myoglobin
Earliest enzyme to elevate after MI Myoglobin
CPK is increased in Alcoholic myopathy, Clofibrate therapy, After
electrocardioversion
Enzyme raised in 4 to 6 hours and decreases in 3 to 4 CPK
days
Heart muscles contain isoenzyme MM and MB
Investigation of choice for second MI after 1 week of CPK-MB
previous MI
Enzyme elevated in first 2 hours of MI CPK MB
Enzyme of choice during reperfusion CK- MB
Best enzyme assay within 3 hours following acute MI CK -MB
Most Sensitive enzyme for Myocardial Infarction Troponin
Biomarker of recurrent MI CKMB
Test of choice in patient coming 12 hours following MI Cardiac troponin
Marker of choice in Myocardial infarction with Troponin I
hypothyroidism
Normal value of troponin T 0 – 0.01 microgram/L (ng/ml)
Troponin T preferable to CPK MB in diagnosis of acute Bedside diagnosis of MI, post operatively after CABG,
MI in small infarcts
Best indicator of MI after 72 hours Cardiac specific troponin T
Troponin T is a marker of Myocardial infarction
Preferred marker of acute STEMI in athletes Troponin T
Troponin T is NOT preferable in Reinfarction after 4 days

DIAGNOSIS IN ISCHEMIC HEART DISEASE

Pain epigastrium, difficulty in breathing, initial ECG

investigation
Feature of acute coronary syndrome ST depression and T wave inversion
ECG is poor in detecting ischemia in areas supplied by Left circumflex artery
ECG finding associated with acute MI Tall T wave with increased amplitude
ST segment elevation Early repolarisation variant, ventricular aneurysm,
prinzmetal angina
ST elevation in II, III, AVF indicates Inferior wall MI
Fresh myocardial infarction in ECG ST segment elevation
ST elevation and hyperacute T waves in precordal leads Anterolateral wall MI
V1 to V6 and in lead aVL
Characteristic ECG finding of transmural myocardial Pathological Q waves
infarction
Most sensitive lead in detecting intraoperative ischemia V5
NOT seen in ECG tracing of MI Biphasic P wave
Coronary angiography can visualize vessels with lumen 0.5 mm

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 MYOCARDIAL INFARCTION 25
CARDIOVASCULAR SYSTEM

up to
Drug used to perform stress echo Dobutamine
Phase of minimum motion during cardiac imaging Mid diastole
Following an attack of MI, mortality and morbidity of a Left ventricular ejection fraction
patient is indicated by
Ischemic cardiac tissue shows Anaerobic Glycolysis
Myocardium Rest injection thallium scan is used in hibernating
myocardium, Late Gd MRI enhancement is suggestive of
scar but Gd scan is not used for hibernating
myocardium detection
Hot spot in acute myocardial infarction Tc99 strontium pyrophosphate
Infarct Avid imaging/Hotspot imaging Myocardial Infarction
Myocardial viability is detected by Thallium scan
Test of choice for reversible Myocardial ischemia Thallium scan
Nuclear cardiac imaging of heart utilizes Thallium
Commonly used thallium Thallium 201
Best time to perform myocardial infarct 12 – 24 hours
imaging with thallium 201
SPECT scan is used for Heart
Bruce protocol for Ischemic heart disease
Modified exercise test 6 days after MI

MANAGEMENT OF MI

Best possible intervention of acute myocardial Early primary coronary intervention

infarction
Drug used for Pain relief in MI Morphine
Low dose aspirin used in myocardial infarction act by Inhibit cycloxygenase
Immediate intervention in ST segment elevation in Aspirin
inferior leads
Reperfusion is believed to restore contractile function Hibernating myocardium
of
Accelerated idioventricular rhythm is most common Myocardial reperfusion
arrhythmia associated with
Chest pain, ST segment depression, NOT given Thrombolytic
Antineoplastic drug best avoided in myocardial Anthracycline
infarction and congestive cardiac failure
Drug contraindicated in acute MI Pentazocine
NOT used in myocardial infarction Inhibitors of plasminogen activator
Drug NOT given in ischemic heart disease Isoproternol
NOT used for intraoperative management of myocardial Heparin
ischemia
NOT used in acute myocardial infarction Calcium channel blocker
NOT a management of Unstable angina/ STEMI Lignocaine bolus
NOT used in management of acute MI Warfarin
Anterior wall MI, RBBB left atrial hypertrophy Temporary pacing
Best treatment for STEMI PTCA
Immediate modality in acute anterior wall MI and Primary angioplasty
hypotension
Percutaneous coronary intervention through Femoral artery

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CARDIOVASCULAR SYSTEM

Fractional flow reserve is used in Coronary catheterization

Most effective management in triple vessel heart CABG
disease
CABG is best indicated in Double vessel disease with CCF
NOT an indication of CABG To prevent progress of native blood vessel disease
Tolazoline Vasodilator in treating coronary artery stenosis during
angio procedure
Tolazoline As vasodilator in treating coronary artery stenosis
during angioprocedures
CABG in NOT done to Prevent progress of native blood vessel disease
Coronary care unit and cancer care facility to be District level hospital
established at the

THROMBOLYSIS

TIMI 0 means Complete occlusion

Thrombolytics can be given in treatment of AMI, if 12 hours
patient comes within
Thrombolysis should be started in Ischemic stroke 3 hours
within for Maximum benefit
Thrombolysis is CONTRAINDICATED IN Non STEMI
NOT a contraindication for thrombolytic therapy Supraventricular tachycardia
Recurrent ischemic events following thrombolysis has Lipoprotein A
been physiologically linked to
Most common cause of death in a patient with Intracranial hemorrhage
thrombolytic therapy?
Widely used thrombolytic agent Streptokinase
Commercial source of streptokinase S. dysgalactiae (subspecies equisimilus)
Streptokinase and urokinase are contraindicated in Intracranial malignancy
Complications of streptokinase Intracranial bleed, fever, anaphylaxis, hypotension
Bolus fibrinolytics Tenecteplase, Reteplase
Plasminogen activator produced by recombinant DNA Alteplase
technology

WARFARIN

Anticoagulant action of warfarin is monitored by PT

Treatment of warfarin toxicity Phytonadione

AORTIC DISSECTION
Cardiovascular causes of clubbing Infective endocarditis, AV fistula, tricuspid atresia
Digital clubbing NOT seen in Aortic dissection
Factors predisposing to aortic dissection Systemic hypertension, Coarctation of aorta, Takayasu
arteritis, Marfan syndrome

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 ARRHYTHMIAS 27
CARDIOVASCULAR SYSTEM

MC cause of dissecting aneurysm of thoracic aorta Medial degeneration

MC cause of abdominal aortic aneurysm Atherosclerosis
Dissection of which artery is common in pregnancy Aorta
MC site of aortic dissection Ascending aorta
MC site of aortic dissection Near aortic valve
Sudden onset of excruciating pain, radiating to back, Dissecting aneurysm of aorta
shock, distension of abdomen, mild rigidity,
precipitated by exertion
Manifestation of acute aortic dissection Pericardial effusion, AR, AMI, limb ischemia
Apical cap on chest X ray Dissecting aneurysm
Abdominal aortic aneurysm may be complicated by Occlusion of artery of adamkiewicz
Severe back pain in abdominal aortic aneurysm Enlargement of sac
Most common complication of aortic aneurysm of size 8 Rupture
cm
Most common site of rupture of abdominal artery Laterally into left retroperitoneum (infrarenal)
aneurysm
Abdominal aortic rupture usually Posterolaterally
ruptures
Stanford classification for Aortic dissection
Investigation of choice for Aortic Dissection(Stable) MRI
Investigation of choice for Aortic Dissection(Unstable) Transesophageal ECHO followed by CT
Diameter of aortic aneurysm is best described by MRI
Procedure of choice for evaluating aneurysm Arteriography
Fibroptic endoscopy contraindicated in Aneurysm of arch of aorta
Treatment of aortic dissection Propanolol, sodium nitroprusside, labetalol
Bentall’s procedure is for Aortic root aneurysm repair
Criteria for endovascular repair of Asymptomatic infrarenal or common iliac
aneurysm aneurysm, anatomy suitable for repair,
aneurysm neck length > 10 mm, external
and common iliac arteries must
accommodate the device

ARRHYTHMIAS

CARDIAC CONDUCTION

Resting membrane potential of sino nodal -55 mV

fibres
SA node Situated at junction of SVC and right atrium, Contains
specializes nodal cardiac muscle, Initiates cardiac
conduction
SA node No t tubule
Sinus arrhythmia is produced by SA node
Slow depolarizing pre potentials are characteristic of SA node
SA node is pacemaker because its excitability is Highest of all
SA node acts as pacemaker because It generates impulses at highest rate
Blood supply to SA node Right posterior interventricular artery

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 ARRHYTHMIAS 28
CARDIOVASCULAR SYSTEM

Right posterior interventricular artery is Middle cardiac vein

accompanied by
Resting membrane potential of -90mV
myocardial fibers
Initial depolarization is due to Rapid Na+ influx
Plateau phase is due to Slow Na+ influx
Repolarization is due to K+ efflux
Action potential in SA node and AV node Ca++ influx
owing to
Initiation of prepotential in cardiac Closure of K+ channel
pacemaker is due to
Vagal stimulation on membrane potential Activates hyperpolarizing potassium
of SA node current
Stronger than normal stimulus cause Relative refractory period
excitation during
Refractory period is NOT affected by Sympathetic stimulation
Pacemaker potential or prepotential Decrease in K+ permeability
Prepotentials are normally absent in Purkinje fibres, working myocardial cells
Predepolarisation phase of SA node action potential is Ca++ entry
due to
Slowest conduction velocity Atrial myocardial fibres
Least conduction velocity seen in AV node
Decremental conduction is associated with AV node
AV bundle is related to Membranous part of ventricular septum
Right coronary artery supplies AV node 60% of individuals
in
Atrioventricular Nodal delay is due to Resistance to Ion flow
AV nodal delay is increased by Stimulation of left vagus
Ability of AV node to generate its own Spontaneous diastolic depolarization
impulse when sinus node is sick
Fibres from AV node to RV Moderator band
Fibres from AV node to fascicles Mahaim fibres
AH interval (conduction time from atria 60 – 125 ms
to His bundle)
Maximum velocity of Transmission in heart in Bundle of His
Conduction rate is fastest in Purkinje fibres
Order of activation after stimulation of Purkinje system Septum > Endocardium > epicardium
Repolarisation in isolated muscle pierce fibre from Endocardium to epicardium
Plateau phase of ventricular muscle is due to opening of Ca – Na channel
Principal determinant of inotrophic state of heart Intracytoplasmic Ca++
Extrasystole in ventricle Falls to produce radial pulse, Associated with abnormal
QRS complex, Tendency to be followed by a
compensatory pause
NOT true about extrasystole Hints at serious heart problem
Patient develops sudden palpitation HR 150/min Sinus tachycardia
Bradycardia is caused by Propanolol, clonidine, reserpine
Management of Severe bradycardia Atropine, pacing, isoproterenol
Should be given safely in patients with sinus Esmolol

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 ARRHYTHMIAS 29
CARDIOVASCULAR SYSTEM

bradycardia
Asystole Absence of cardiac conduction > 2000 ms
Fibrocalcareous encroachment into the conducting Lev’s disease
system
Ashman phenomenon is seen with Atrial fibrillation (right bundle branch block)
Left bundle branch block Coronary heart disease, hypertensive heart disease, aortic
valvular disease, cardiomyopathy

GENERAL FEATURES OF ARRHYTHMIA

Patient taking ketaconazole and terfenadine prone for Cardiac arrhythmia

MC mechanism of arrhythmia Re entry
MC cause for extrinsic SA node dysfunction Drugs
SA node dysfunction is associated with Kearns Sayre syndrome
Tachycardia bradycardia syndrome Autosomal dominant SA nodal dysfunction syndrome
Transient SA node dysfunction is associated with Inferior wall MI
Frog sign AV nodal reentrant tachycardia
Pseudo R waves are associated with AV nodal reentrant tachycardia
Epsilon wave is associated with Arrhythmogenic right ventricular dysplasia
Naxos disease Arrhythmogenic right ventricular dysplasia/cardiomyopathy,
woolly hair, palmoplantar keratosis
Cyclic variation of heart rate Sinus arrhythmia
Respiratory sinus arrhythmia Decrease in heart rate during expiration
and increase in heart rate during
inspiration, abolished by atropine, reduced
in elderly

ATRIAL FLUTTER

Arrhythmia commonly associated with alcohol binge in Atrial flutter

alcoholics
Drug most useful in atrial flutter Amiodarone
Most effective treatment of Atrial flutter DC shock

ATRIAL FIBRILLATION

MC arrhythmia associated with alcohol binge in Atrial fibrillation

alcoholics
Atrial fibrillation is due to Thyrotoxicosis
Atrial fibrillation Mitral stenosis, constrictive pericarditis, diphtheritic
myocarditis
Atrial fibrillation does NOT occur in Hypothyroidism
Irregularly irregular pulse Atrial fibrillation
Known mitral stenosis, atrial fibrillation, acute onset of Ischemic stroke
weakness rcovered completely in 2 weeks
NOT true about atrial fibrillation Anticoagulant NOT required
P waves are absent in Atrial fibrillation

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CARDIOVASCULAR SYSTEM

Treatment of resistant cases of Atrial fibrillation Amiodarone

Drug of choice in wolf parkinson’s syndrome with atrial Procainamide
fibrillation
Digitalis has most profound effect in Atrial fibrillation
Purpose of digitalis in atrial fibrillation Slow ventricular rate
Vernalakant is used in treatment of Atrial fibrillation
Drug of choice for ectopic atrial Amiodarone
tachycardia
Most effective for conversion of atrial Amiodarone
fibrillation to sinus rhythm
Most effective treatment of atrial fibrillation DC shock
NOT used in Atrial arrhythmia Lignocaine
Maze operation is done for Atrial fibrillation

VENTRICULAR TACHYCARDIA

Most common type of surpaventricular AVRT

tachycardia in infants
Type of SVT Wolff Parkinson White Syndrome
Features of ventricular tachycardia Variable first heart sound, Can NOT be relieved by
carotid sinus massage, QRS duration >0.14 sec
Patient with wide complex tachycardia, which indicates AV dissociation, fusion beats, capture beats
ventricular tachycardia
Ventricular tachycardia Fusion beat, Capture beat, AV dissociation, Bizzare QRS
complexes
Repolarization alterans is seen in Ventricular tachyarrhythmia
NOT true about ventricular tachycardia Similar QRS in all leads
Treatment of Ventricular Tachycardia Lignocaine
Tocainide Used in ventricular tachycardia, used as lidocaine
analogue, orally
Heart rate is slowed by Carotid massage
Used for treatment of supraventricular tachycardia with Carotid sinus massage, adenosine, direct current
hypotension under general anesthesia cardioversion
Mechanism of abruption of SVT by Increase parasympathetic discharge to SA
cardiac massage node
Drug of choice for PSVT Adenosine,Verapamil
Drug of choice in most cases of acute AV nodal Adenosine
tachycardia
Adenosine Used in PSVT, administered as rapid iv infusion, short
lived side effects
Adenosine Dipyridamole potentiates action, Used to produce
controlled hypotension
Arrhythmias that can be treated with Adenosine Atrial flutter, Paroxysmal atrial tachycardia,
supraventricular tachycardia
PSVT Rapid Control in Known Asthmatic Verapamil
Treatment of antipsychotic induced ventricular Sodium bicarbonate
tachydysrhthmia
Drug of choice for ventricular Amiodarone

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CARDIOVASCULAR SYSTEM

tachycardia during cardiac arrest

Digitalis is contraindicated in Ventricular tachycardia

VENTRICULAR FIBRILLATION

MC electrical mechanism for cardiac arrest Ventricular fibrillation

MC cause of Sudden Cardiac Death Ventricular Fibrillation
MC cause of death from Aortic stenosis in children Ischemic heart disease with Ventricular fibrillation
MC cause of death from chloroform anaesthesia Ventricular fibrillation
Ventricular fibrillation is associated with Follows ventricular tachycardia, quick fall in cardiac
output
VF is treated by Lignocaine
Drug of choice for ventricular arrhythmia due to MI Xylocaine
First line of treatment if a patient develops ventricular Defibrillation
fibrillation after intravenous infusion of potassium
chloride
Treatment of Ventricular fibrillation Immediate electrical cardiac version

MANAGEMENT OF ARRHYTHMIA

Class IA antiarrhythmic (Na+ K+ blocker) Quinidine, procainamide, disopyramide

Quinidine Class IA antiarrhythmic
Quinidine is a Na+ blocker
Quinidine exerts its action on heart by inhibiting Na+ channel
Quinidine Decreases automaticity in heart
Quinidine Increases effective refractory period, Paradoxical
tachycardia, Cinchonism is seen
Quinidine is contraindicated in Bifascicular block, acute carditis, thyrotoxicosis
Effective refractory period is prolonged by Propanolol, Verapamil, Lignocaine
Procainamide Class I antiarrhythmic
Class IB antiarrhythmic (Na+ blocker K+ Lignocaine, phenytoin, mexilentene,
opener) tocainamide
Mexiletine Class IB antiarrhythmic
Lignocaine Class IB antiarrhythmic
Anti arrhythmic drug decreases action potential Lignocaine
duration is purkinje fibres
Antiarrhythmic NOT proarrhythmic Lignocaine
Antiarrhythmic drugs which are NOT proarrhythmic Verapamil, diltiazem, moricizine
Class IC antiarrhythmic (Na+ blocker) Flecainadine, encainidine, propafenone,
moricizine
Does NOT belong class IC antiarrhythmic Tocainide
Feature of class IC anti arrhythmic agents Pro arrhythmic
Esmolol Class II antiarrhythmic
Beta blockers are antiarrhythmogenic agents of type II
Sotalol Non selective beta blocker, prolongs action potential
duration throughout heart, polymorphic ventricular
tachycardia is a common side effect, excreted
unchanged in urine

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CARDIOVASCULAR SYSTEM

Sotalol excreted mainly by Kidney

Class III (K+ blocker) Amiodarone, bretylium, ibutilide
Anti arrhythmic least likely to cause Amiodarone
torsades de pointes
Amiodarane Class III antiarrhythmic
Action of amiodarone Action potential duration is prolonged, effective
refractory period is prolonged, conduction is slowed
Antiarrhythmic drug cause prolonged repolarisation of Amiodarone
ventricles and ERP
Arrhythmias refractory to treatment of lignocaine can Amiodarone
be treated by
Dronedarone Shown to reduce hospitalization in
patients with AF
Side effects of amiodarone Pulmonary fibrosis, Hypothyroidism, Hyperthyroidism,
Corneal microdeposits, Cirrhosis of liver
NOT an adverse effect of chronic amiodarone therapy SLE
NOT seen with amiodarone therapy Productive cough
Dilitazem Class IV antiarrhythmic
Verapamil Class IV antiarrhythmic

HEART BLOCK

Bifascicular block LBBB and RBBB

Trifascicular block Alternating RBBB with LBBB
Constant PR interval First degree block, Mobitz type II second degree block
Earliest sign of diphtheric myocarditis First degree AV block
st
Treatment of 1 Degree AV block Atropine
Digoxin classically causes Mobitz type 1 block
Mobitz type I block Varying PR interval, Normal QRS morphology, Regular
Atrial rhythm, Atrial rate > Ventricular rate
Type I second degree block Progressive prolonging PR interval
Wenkebach phenomenon is seen in II degree AV block Mobitz type I
2nd Degree AV block Type I Atropine
Type II block Intermittent failure of conduction, associated with
paroxysmal AV block
Stroke Adams attack occurs II degree AV block Mobitz type II
nd
2 Degree AV block Type II Temporary Pacemaker
Atenolol is NOT indicated in Partial heart block
Child born to SLE mother Heart block
Anti SSA(Rho) & Anti SSB(La) Congenital Heart Block
History of Stroke Adam’s attacks, giddiness, Collapse Unstable block
AV nodal block Clinical evidence of inferior MI, wenkebach periodicity
of conduction, escape focus rate faster than 50 beats
per minute
Symptoms of cerebral ischemia is Infranodal block
associated with
Treatment of Complete Heart Block Permanent Pacemaker
Treatment of choice in symptomatic sinus node Permanent pacemaker
dysfunction

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CARDIOVASCULAR SYSTEM

Pacemaker therapy is indicated in Congenital AV block, trifascicular block, sick sinus

syndrome
Twiddler syndrome Rotation of pacemaker
Acute symptomatic sinus bradycardia usually responds Atropine
to
NOT a modality of treatment in severe bradycardia Diltiazem
ICD means Implantable cardiac defibrillator
Implantable cardiac defibrillator Primary prevention

VENTRICULAR PREMATURE CONTRACTION

Premature ventricular beat Sequential depolarisation of ventricles, Wide bizzare

notched QRS complex, Palpitation is a common
presenting feature, Wide QRS, Absent P wave,
Complete compensatory pause, Fusion beat, Capture
beat, AV dissociation
Most characteristic finding of ventricular premature Wide QRS complex
complex
Ventricular premature complexes are associated with Full compensatory pause
Interpolated VPC VPC without compensatory pause
NOT a feature of ventricular premature complex Narrow QRS complex
Drug of choice for ventricular premature beats due to Diphenylhydantoin
digitalis toxicity
MC arrhythmia encountered in digitalis toxicity Bigeminous rhythm
Proper treatment of ventricular bigeminy Cessation of digitalis and administration of potassium

TORSADES DE POINTES

QT prolongation seen in Hypocalcemia, hypothermia, Romanowand syndrome

Torsades des pointes caused by Quinidine
Torsades de pointes caused by Quinidine, Disopyramide, Procainamide
Drug implicated for prolonging QT interval in premature Cisapride
baby
Co administration of ketoconazole and cisapride cause Torsades de pointes, ventricular fibrillation and
ventricular tachycardia
Cisapride for Barrett’s ulcer. He develops pneumonia. Increased risk of ventricular arrhythmia
Physician prescribes erythromycin
MC type of long QT syndrome LQT1
LQTS1 Stress induced
LQTS3 Sudden death during sleep
Congenital long QT syndrome can lead to Polymorphic ventricular tachycardia
Congenital long QT syndrome is associated with Neonatal sinus bradycardia
Treatment of long QT syndrome Beta blocker
Best treatment for congenital long QT Implantable cardiac defibrillator
syndrome
Feature of Torsades des pointes Prolonged QTc interval
Torsade de pointes Hypomagnesemia
Known prolonged congenital QT syndrome and Metoprolol

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CARDIOVASCULAR SYSTEM

intermittent torsade de pointes

Treatment of Choice for Torsades de pointes Magnesium Sulphate
Tachycardia NOT amenable Torsades de pointes
radiofrequency catheter ablation

WPW SYNDROME

MC accessory pathway Left free wall

WPW syndrome caused by Right sided accessory pathway
WPW syndrome Common in males
WPW syndrome Right ventricular aberrant is commonly seen, incidence
decreases with age, heart is structurally normal
MC reentrant tachycardia associated with WPW Orthodromic AV reentry
syndrome
WPW syndrome is associated with Echo beat (echo wave)
In Wolff Parkinson syndrome connection between Ventricles
atrium and
ECG findings in WPW syndrome Normal QT interval, slurred tall QRS, Short PR interval
Short PR interval with delta waves WPW syndrome
NOT a cardiac contraindication to pregnancy WPW syndrome
Treatment of choice for Wolff Parkinson White Radiofrequency ablation
Syndrome
Asymptomatic child with delta wave short PR interval Beta blocker
which drug not to be given

ATHEROSCLEROSIS

CAUSES OF ATHEROSCLEROSIS

Causative organism for coronary atherosclerosis Chlamydia pneumonia, CMV, Herpes Simplex
Organism implicated in coronary artery disease Chlamydia
Aminoacid associated with atherosclerosis Homocysteine
Increased level of lipoprotein predispose to Atherosclerosis
Risk factors for atherosclerosis Increased homocysteine, increased lipoproteins,
increased fibrinogen, increased plasminogen activator
inhibitors
Atherosclerotic plaque formation is due to Persistent endothelial injury
Increased risk of atherosclerotic plaque formation Apo E mutation, oxidized LDL, increased homocystine
associated with
Susceptibility to coronary artery disease Nephrotic syndrome
Predisposing factors for CAD Homocystinemia, Increased fibrinogen, Increased
plasminogen activator inhibitor
Predispose to atherosclerosis Homocystinemia, Fibrinogen, Lipoprotein A
Drug causing Hyperlipidemia Prednisolone
Highest Risk of CHD is seen in Familial Hypercholesterolemia

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CARDIOVASCULAR SYSTEM

Agatston score is used for Quantification of calcified plaque

NOT a predisposing factor for atherosclerotic plaque Alpha 2 macroglobulin
Metabolic syndrome is associated with Decreased adiponectin
NOT a criteria for metabolic syndrome LDL
NOT a risk factor in IHD Diabetes insipidus
NOT a risk factor for atherosclerosis Decreased fibrinogen levels
Dietary relation not established in CAD K+
Atherosclerosis risk decreased with PUFA intake

FEATURES OF ATHEROSCLEROSIS

MC cause of Renovascular Hypertension in Elderly Atherosclerosis

MC cause of True Aneurysm in India Atherosclerosis
MC cause of Peripheral Limb Ischemia in India Atherosclerosis
MC cause of Abdominal Aortic Aneurysm Atherosclerosis
MC cause of thoracic aortic aneurysm Atherosclerosis
MC cause of Aortic aneurysm Atherosclerosis
MC cause of peripheral limb ischemia in India Atherosclerosis
Chronic smoking pain in lower limb due to obstruction Atherosclerosis
of femoral artery
Atherosclerosis affects Medium and Large sized vessels
Coronary artery most commonly involved in Left anterior descending artery
atherosclerosis
MC site of coronary atherosclerosis Epicardial coronary artery
LEAST common site of atherosclerotic lesions Pulmonary artery trunk
Arteries spared in atherosclerosis Arteries of upper extremity, mesenteric
arteries, renal arteries
Elderly man with fusiform dilatation of descending Atherosclerosis
aorta because of
Mortality in emergency abdominal aneurysm repair >50%

MORPHOLOGY IN ATHEROSCLEROSIS

Thush breast / tigered effect Fatty change in heart

Characteristic lesion of atherosclerosis Fibrofatty lesion in intima of blood vessel
In atherosclerosis, increased LDL in monocyte Lipids in LDL gets auto oxidized
macrophage is due to
Pathophysiological phenomenon that occurs during Calcium deposition in atheromatous plaque
atheromatous plaque formation and is used for
screening of asymptomatic coronary plaque
Atheromatous Plaques do NOT contain Neutrophils

DIAGNOSIS OF ATHEROSCLEROSIS

Marker to predict serum atherosclerosis in early age Apoprotein B100

Raised serum level of lipoprotein A is a predictor of Atherosclerosis

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CARDIOVASCULAR SYSTEM

Best predictor for future risk of cardiovascular events Hs CRP

Triglyceride level risk for IHD >150
Best marker for dyslipidemia LDL/HDL ratio
Best predictor of risk of developing cardiovascular LDL/HDL ratio
disease
Most important in causing coronary artery disease LDL
LDL is checked by Skin fibroblast culture
Most important predictor of coronary artery disease HDL
Lipoprotein acting as a scavenger and preventing HDL
atherosclerosis
Protective against atherosclerosis HDL
Inverse relation for increasing risk of Atherosclerosis HDL
Coronary calcium is quantified by Agatston scoring

HYPOLIPIDEMIC DRUGS

HDL specifically increased by Niacin

Favourable lipid profile is provided by Nicotinic acid
Nicotinic acid Decreases VLDL product
HDL levels are increased by Nicotinic acid
In a patient with poor glycemic control, Nicotinic acid
hypertriglyceridemia, low HDL, which drug will be best
without myositis as side effect
Class of hypolipidemic drug used safely in Niacin
pregnancy
Laropiprant is used with Niacin
Drug contraindicated in severe hypertriglyceridemia Niacin
Most potent drug to reduce plasma cholesterol level Statins
First step in cholesterol synthesis inhibited by Statins
HMG CoA reductase inhibitors CNS accumulation of simvastatin and lovastatin is high
and less for pravastatin and fluvastatin, Simvastatin is
rapidly and pravastatin is least metabolized,
Bioavailability is minimally modified when pravastatin is
taken with food
HMG coA reductase inhibitors CNS accumulation of simvastatin and lovastatin is high
and less for provastatin and fluvastatin, simvastatin is
rapidly metabolized and provastatin is least,
bioavailability is minimally modified when provastatin is
taken with food, fibrinogen levels are decreased by
provastatin
Statins on HDL Increases
Lovastatin HMG CoA reductase inhibitor
Chinese yeast rice contains substance having action of Lovastatin
Pravastatin Decrease fibrinogen levels
Severe myopathy is a common side effect of Rosuvastatin
Grape juice should not be given to patients on Atorvastatin
First step in cholesterol synthesis inhibited by Lovastatin
Teratogenicity of statins VACTREL
Fibrates Increase lipoprotein lipase activity through PPAR alpha
and cause increased lipolysis of triglycerides, cause

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CARDIOVASCULAR SYSTEM

utricaria, rash, alopecia, myopathy, GI distress, first line

of drugs in severe dysbetalipoproteinemia and
hypertriglyceridemia, absorption increased when taken
with food
Fibrates Absorbed good when taken with food, Drug of choice
for type III hyperlipoproteinemia and severe
hypertriglyceridemia, Activate PPAR to stimulate LPL
Side effects are rash, utricaria, myalgia
Newer fibrates Can be given with or without food
Action of clofibrate Activating lipoprotein lipase resulting in VLDL
degradation
Fibrates are contraindicated in Gall stones
Drug used in treatment of hypertriglyceridemia in Gemfibrozil
primary stage
Ezetimibe acts by Decreased absorption of cholesterol
Drug reducing cholesterol levels by reducing cholesterol Ezetimibe
absorption in intestine by acting on NPC1L1 receptor
Ezetimibe Inhibition of Intestinal cholesterol absorption
Probuchol Inhibition of LDL oxidation
Cholestyramine Basic ion exchange resin, cause compensatory increase
in HMG CoA reductase activity, may cause constipation,
steatorrhoea
INH can be used in CAD
Icosapent is used in treatment of Hyperlipidemia

PREVENTION OF ATHEROSCLEROSIS

HDL in CAD should not be less than 32

Effect of omega 3 fatty acids Increased LDL, decreased cholesterol
NOT a dietary goal in patient with risk of coronary heart Avoid alcohol
disease

CARDIAC TUMOURS

Cardiac polyp Fibrinous clot

Cardiac tumor in childhood Rhabdomyoma, Myxoma, fibroma
MC Cardiac tumor of Children Rhabdomyoma
MC tumor of infancy Rhabdomyoma
MC soft tissue tumor in child Rhabdomyosarcoma
Marker of Rhabdomyosarcoma Desmin
MC tumor of cardiac valves Papillary fibroelastoma
NAME syndrome Nevi, Atrial myxoma, Myxoid neurofibroma, Ephelide
MC Primary cardiac tumour of Adults Myxoma
MC primary tumour of heart Myxoma
MC intracavitary benign cardiac tumour Myxoma
Cardiac myxoma common in Left atrium
Favoured site of origin of Myxoma Fossa ovalis in atrial septum

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CARDIOVASCULAR SYSTEM

Features of Myxoma Fever, clubbing, embolic phenomenon

Blue naevi and Multiple lentigenes associated with Atrial myxoma
Lipidic cells Myxoma of heart
Substance accumulated in Cardiac Myxoma Mucopolysaccharides
Gradient in pulmonary artery wedge pressure and left Left atrial myxoma
ventricular end diastolic pressure is seen in
Atrial myxoma may mimic Infective endocarditis
NOT true about myxoma Hypertension, familial
Intracardiac mass is detected by 2D TTE

RHEUMATIC FEVER

FEATURES OF RHEUMATIC FEVER

Serotype frequently associated with M5

Rheumatic fever in India
MC cause of acquired heart disease Acute rheumatic heart disease
Percentage of coincidence between Sore throat and 3%
Acute Rheumatic fever
Rheumatic fever Caused by beta hemolytic streptococci
Age group for Rheumatic fever 5 – 15 years
Mechanism of acute rheumatic fever Cross infectivity endogenous antigen
Mechanism of autoimmunity in rheumatic Molecular mimicry
fever
MC Site of Rheumatic Fever Vegetations Mitral > Mitral + Aortic
Valve least affected in rheumatic fever Pulmonary
Rheumatic fever Joint pain, ST segment elevation, increased PR interval,
cardiomegaly
Rheumatic fever in children Polyarthritis, mitral valve commonly affected
Characteristic manifestation of cardiac involvement in Pancarditis
Rheumatic fever
Marker for carditis in rheumatic fever Subcutaneous nodules
MC cause of enlarged cardiac shadow in X ray of child Rheumatic carditis
NOT a definite sign of carditis Prolonged fever
Carey coomb murmur Low pitched murmur, Seen in rheumatic fever
Low pitched delayed Diastolic Murmur in Rheumatic Carey Coomb murmur
Fever
Carey Coomb murmur of Rheumatic carditis Apical Mid diastolic murmur
Rheumatic fever Chorea aggravated during pregnancy
Syndemham’s chorea Triad of emotional liability,
uncoordinated movements, muscle
weakness (hypotonia).
Tongue in syndenham’s chorea Bag of worms
Configuration of hands Extended, dish configuration, milkmaid
grip

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CARDIOVASCULAR SYSTEM

NOT true about Rheumatic chorea in children Within 8 -12 weeks of disease
Manifestation of Rheumatic fever disappears Arthritis
completely
Subcutaneous nodule in rheumatic fever Tender
Rheumatic nodules Rarely occur unless active carditis is present
Subcutaneous nodule in rheumatic fever Non tender, usually located on extensor aspect
Erythema marginatum in acute rheumatic fever Usually associated with carditis
Smoke rings beneath skin Erythema marginatum
PANDAS Pediatric autoimmune neuropsychiatric
disorder associated with streptococci, tics,
OCD, diagnosis made rarely in high
incidence RF
NOT a major manifestation of Acute rheumatic fever Fever, ESR
NOT included in Jones major criteria High ESR
NOT true about rheumatic fever Communicable disease
NOT true about rheumatic fever Communicable disease
NOT true about epidemiology of RHD Mitral regurgitation is commonest cardiac lesion

CRITERIA OF RHEUMATIC FEVER

NOT a criteria for acute rheumatic fever Erythema nodosum

Major criteria Chorea, arthritis, carditis
NOT a major criteria for Rheumatic fever Increased CRP
NOT a major criteria for Rheumatic fever Prolonged PR interval
Minor criteria of rheumatic fever according to modifies Fever
Jones criteria

MORPHOLOGY OF RHEUMATIC FEVER

Rheumatic heart disease Aschoff nodule(seen in any of the layer), McCallum

patch, fibrinous pericarditis
Fine warty vegetations along the line of closure of Rheumatic heart disease
valves is due to
Exudative in Rheumatic fever is Fibrinous
Vegetations in rheumatic heart disease Along line of closure
Calcification of heart wall Endomyocardial fibrosis
Intracardial calcification involves Rheumatic valves
Fibrinoid necrosis due to Rheumatic fever occurs in Endocardium
Anitchkow cells are pathogonomic of Acute rheumatic fever
Most distinctive lesion in rheumatic fever Aschoff bodies
Aschoff Bodies Pathogonomic of Rheumatic Fever
Aschoff bodies constitute foci of swollen eosinophilic Lymphocytes and monocytes
collagen surrounded by
Aschoff body in rheumatic heart disease does NOT Epitheloid cells
show
McCallum patch is seen in Rheumatic fever (Left atrium)
McCallum plaques are seen in Left atrium

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CARDIOVASCULAR SYSTEM

DIAGNOSIS OF RHEUMATIC FEVER

Acute phase reactants in rheumatic fever 12 weeks

is elevated for
Most common serologic test for RF ASO and Anti DNAase B
Confirmation of Rheumatic fever ASLO Titre
A child comes with migratory polyarthritis, investigation ASLO titre
of choice to confirm diagnosis
Diagnosis of rheumatic fever is best confirmed by ASLO
Rheumatic fever is diagnosed by presence of ECG evidence of prolonged PR interval

MANAGEMENT OF RHEUMATIC FEVER

Drug of choice for syndenham’s chorea Phenobarbitone

Drug of choice to suppress lactation in mother with Pyridoxine
Rheumatic fever
Treatment of aspirin resistant rheumatic Naproxen
fever
Treatment of penicillin allergy rheumatic Sulfadiazine
fever
Drug of choice for rheumatic fever prophylaxis in Erythromycin
penicillin allergic patient
Course of full dose steroids in Rheumatic carditis 3 weeks
Acute rheumatic carditis with fever Valve replacement will ameliorate CCF
Jai Vigyan mission project for RF/RHD in India, involves
epidemiological studies, registration and
vaccine development

CARDIOMYOPATHY

FEATURES OF CARDIOMYOPATHY

Keshan Disease Endemic cardiomyopathy, Deficiency of Selenium

Mineral associated with cardiomyopathy Cobalt chloride
Cardiomyopathy is associated with Ducchne muscular dystrophy, Friedrich ataxia, Type II
glycogen storage disese
Cardiomyopathy is associated with Barth syndrome (mutation in tafazzin gene), Glycogen
storage disease type II and III, HCV, Chaga’s disease
Trastuzumab Cardiomyopathy
Doxorubicin Causes Cardiomyopathy >550 mg/m2
Cardiomyopathy NOT seen in Alkaptonuria
Cardiomyopathy is NOT a feature of Lowe syndrome
Tako Tsubo cardiomyopathy Global ventricular enlargement, basal constriction, shape of

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CARDIOVASCULAR SYSTEM

narrow necked jar, also known as apical ballooning

syndrome
Tako tsubo cardiomyopathy Females are affected, coronary artery is
normal, hypokinesia on ECHO,
management is with beta blockers

DILATED CARDIOMYOPATHY

Beta adrenoceptor has been implicated as Dilated cardiomyopathy

an autoanigen in pathogenesis of
Mutation in dilated cardiomyopathy Tafazzin
MC cause of cardiac transplantation in Dilated cardiomyopathy
pediatric patients
MC type of cardiomyopathy Dilated cardiomyopathy
Dicrotic pulse Dilated cardiomyopathy
Contractile dysfunction is a dominant feature of Dilated cardiomyopathy
NOT true about alcoholic cardiomyopathy Systemic vasodilatation
Important investigation must be Coronary artery angiography
performed before a diagnosis of dilated
cardiomyopathy

RESTRICTIVE CARDIOMYOPATHY

Least common cause of cardiomyopathy Restrictive cardiomyopathy

MC cause of restrictive cardiomyopathy Amyloidosis
Kussmaul sign Restrictive cardiomyopathy
Restrictive cardiomyopathy differentiated from Diastolic pressures are equalized, Thick pericardium
constrictive pericarditis by

HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY

Mode of inheritance of HOCM Autosomal dominant with complete penetrance

Recurrent chest pain, intensity increased by HOCM
nitroglycerine
Died while playing. autopsy, myocyte hypertrophy HOCM
Pathology is HOCM Diastolic dysfunction
Outflow Obstruction, Dilatation of Atria and Hypertrophic Obstructive Cardiomyopathy
Asymmetrical septal Hypertrophy
HOCM Asymmetrical hypertrophy of septum, dynamic LV
outflow obstruction, double apical impulse
Feature of HOCM Myocardial hypertrophy without
ventricular dilatation
Disrangement of myofibrils is found in Hypertrophic cardiomyopathy
HOCM Double/Triple apical impulse, Diamond shaped murmur
HOCM Crescendo decrescendo systolic murmur, Brisk carotid
upstroke, Increase in murmur during valsalva or

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CARDIOVASCULAR SYSTEM

standing
Harsh systolic murmur of HOCM Does NOT radiate to neck, DECREASE with hand grip
Valsalva maneuver increases loudness of murmur in Hypertrophic cardiomyopathy
Systolic ejection murmur in HOCM is disseminated Squatting
when a patient
Murmur of HOCM decreased in Supine position
Brockenbrough Braunwald sign HOCM
Aggravation of symptoms of angina when nitrates are HOCM
given
Noonan syndrome associated with Hypertrophic cardiomyopathy
Echocardiography features of HOCM Systolic anterior motion of mitral valve (SAM), spade like
appearance
Idiopathic HOCM is associated with Ground glass pattern
HOCM associated with Friedrich’s ataxia No disarray
Drug of choice for Hypertrophic Obstructive β – blocker
Cardiomyopathy
NOT true about HOCM Beta agonists are useful
Digoxin is contraindicated in Hypertrophic obstructive cardiomyopathy
Contraindication of Digoxin Hypertrophic cardiomyopathy
Digoxin & Nitrates are CONTRAINDICATED in HOCM

CONGENITAL HEART DISEASE

FEATURES OF CONGENITAL HEART DISEASE

MC congenital cyanotic heart disease TOF

Least common cause of heart disease in India Congenital
MC Mode of Inheritance in Congenital Heart Disease Multifactorial
MC type of congenital heart disease seen in adults Bicuspid aortic valve
MC type of bicuspid aortic valve Valvular aortic stenosis
Cause of death in congenital heart disease Birth to 7 Pulmonary, Mitral & Aortic atresia
hours
Cause of death in congenital heart disease Hypoplastic left and right heart syndrome,
Transposition & Malposition of Great arteries
Best to declare the case as interatrial septal defect Elevated pressure in right atrium
rather than other cardiac abnormalities
Congenital heart disease which cause death in first Hypoplastic left ventricle
week of life
7 days child, severe respiratory distress and shock. Hypoplastic left heart syndrome
discharged 2 days back healthy
Surgery for Hypoplastic left heart Nortwood
syndrome
Syndrome best associated with congenital heart disease Holt Oram syndrome
Unapposable fingerized thumb Holt Oram syndrome
Congenital defect existing without any manifestation Dextrocardia
Absence of conotruncal septum gives rise Patent truncus arteriosus
to

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CARDIOVASCULAR SYSTEM

Right sided aortic arch is most strongly associated with Truncus arteriosus
NADA’s criteria Assessment of children for presence of heart disease
Least clinical significance Incompetent patent foramen ovale
Taussg Bing anomaly DORV with TGA
A taussig bing malformation is best treated by Diversion of septal defect
Pulmonary plethora is seen in Truncus arteriosus, TAPVC, VSD
Pulmonary plethora Diameter of descending pulmonary artery > 16 mm
In a patient with pulmonary plethora due to left to right VSD
stunt, large left atrium and normal aorta
In a patient with pulmonary plethora due to left to right PDA
stunt, large left atrium and large aorta
In a patient with pulmonary plethora due to left to right ASD
stunt, small left atrium and normal aorta
Objective sign of identifying pulmonary plethora in a Diameter of descending right pulmonary artery > 16
chest radiograph mm
Lung fields are oligemic in TOF, Tricuspid atresia, Ebstein anomaly, single ventricle
with pulmonary stenosis
Ductus arteriosus dependent flow is mandatory for Hypoplastic left heart, TGA with intact ventricular
septum, obliterated aortic arch
Duct dependent systemic circulation All left sided obstructive lesions
Duct dependent pulmonary circulation All right sided obstructive lesions
Duct independent condition TAPVC, Truncus arteriosus, ALCAPA
Congenital heart diseases associated with loud s3 ASD,VSD,PDA
Right axis deviation ASD, VSD, Pulmonary atresia
Right axis deviation is associated with TOF, TGA, TAPVC
Left axis deviation is associated with TA, PA with intact IVS
Flask shaped heart Ebstein anomaly, Tetrology of fallot, Transposition of
great vessels
Newborn cyanosis, oligemic lung field normal sized Pulmonary atresia
heart
Cyanosis is seen in Tricuspid atresia, Eisenmenger complex, TOF
Brain abscess in cyanotic heart disease Parietal lobe
Cyanosis, blood from peripheral vein observed to be Methemoglobinemia
chocolate brown colour
Uhl’s anomaly Aplasia of right ventricular muscle
Apert syndrome is associated with VSD
VATER syndrome is associated with VSD
Crouzon syndrome is associated with PDA, Coarctation of aorta
Incontinenta pigmenti is associated with PDA
Cockayne syndrome is associated with Accelerated atherosclerosis
CHARGE syndrome is associated with TOF
CHARGE syndrome Choanal atresia, coloboma of eye, ear
anomalies
Pallid spell Child becomes pale

TETRALOGY OF FALLOT

NOT true about trilogy of fallot VSD

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CARDIOVASCULAR SYSTEM

Unequal division of conus cordis resulting from anterior Tetrology of fallot

displacement of conotruncal septum gives rise to
Fallot’s tetrology present with Central cyanosis and clubbing
TOF presents with Central cyanosis with clubbing
Clubbing TOF
Boot shaped heart Tetralogy of Fallot
Pulmonary Oligemia Fallot’s tetrology
Couer en sabot Tetrology of fallot
S1 in TOF Normal
TOF Ejection systolic murmur in second intercostal space,
single second heart sound, normal JVP
Systolic murmur in TOF is due to Pulmonic stenosis
TOF Squatting relieves pain, Cyanosis, O2, morphine useful,
LVH
Tetrology of Fallot MC association of Right sided aortic arch
Anoxic spells in TOF is precipitated by Fever, Exertion, Crying of feeding
Pink fallot TOF with mild pulmonary outflow
obstruction
Rare complication of TOF Congestive cardiac failure
Recurrent respiratory tract infection does NOT occur in Tetrology of fallot
NOT an essential criteria for TOF Valvular stenosis
NOT a feature of Tetralogy of fallot Atrial septal defect
NOT true regarding Tetralogy of fallot Predominantly left to right shunt
Condition NOT associated with cardiac arrest Tetrology of Fallot
NOT a potentially treatable cause of cardiac arrest Tetrology of fallot
Reversal of shunt is NOT associated with TOF
Radiological features of TOF Prominent cardiac apex, Prominent Pulmonary bay,
Normal right atrial shadow
Treatment of cyanotic spell Sudden abdominal aortic compression by
applying clenched fist per abdomen
Drug AVOIDED in Tetrology of Fallot with cyanotic spells Isoprenaline
Drug NOT used in treatment of cyanotic Calcium chloride
spell
Oxygen therapy does NOT correct cyanosis in Fallot’s tetralogy
Blalock Taussing shunt between Subclavian and pulmonary artery
Potts shunt Descending aorta to left pulmonary artery
Waterson shunt Ascending aorta to pulmonary artery

ATRIAL SEPTAL DEFECT

MC Heart disease in Pregnancy in Developed countries ASD

Congenital heart disease asymptomatic till adult life ASD
Non syndromic ASD is due to mutation in NKX 2.5
ASD is seen with Ellis van creveld syndrome, Down’s syndrome, Holt
Oram syndrome
Component of pentology of fallot Atrial septal defect
MC cause of ASD Ostium Secondum
MC type of ASD Septum Secundum

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CARDIOVASCULAR SYSTEM

Secundum ASD is associated with Holt Oram syndrome

Primum ASD is associated with Goose neck defect of AV valves
Holt Oram syndrome is associated with Thumb hypoplasia
ASD Left parasternal heave is due to increased pulmonary
artery flow
Presence of pansystolic murmur of mitral regurgitation Ostium primum with floppy mitral valve
in a patient with ASD
ASD with murmur similar to MR and LAD on ECG is Ostium primum defect
having
Aorta in ASD is Small
Bacterial endocarditis is rarely seen in Ostium secundum ASD
Infective Endocarditis NOT seen in ASD
Left atrium NOT enlarged in ASD
Heart lesion NOT found in Congenital rubella infection ASD
NOT true about ASD Left atrial hypertrophy
Does NOT produce cyanosis in first year of life ASD
Great Hilar Dance (Pulmonary Plethora) On Fluoroscopy ASD
Characteristic X ray finding in ASD Pulmonary plethora
Contraindication for ASD operation Severe pulmonary arterial hypertension

VENTRICULAR SEPTAL DEFECT

MC Type of Congenital Heart Disease VSD

MC Congenital Lesion complicated by Infective VSD
Endocarditis
Cardiac anomaly most commonly seen in Down’s VSD
syndrome
A patient with VSD develops pulmonary hypertension, Cyanosis
characteristic feature
A 29 day old child presents with features of congestive VSD
cardiac failure and left ventricular hypertrophy.
auscultation shows short systolic murmur
A child with perimembranous VSD has congestive heart Vascular changes in pulmonary circulation
failure. cause of improvement of cardiac failure in this
patient
Type of VSD associated with aortic Supracristal type
regurgitation
Management of supracristal type Surgery irrespective of size
Cornelia de lange VSD
Katz Watchal phenomenon Equiphasic QRS complex on non
restrictive VSD
Maladie de Roger Defect Small VSD
CCF in perimembranous VSD is due to Changes is Pulmonary vasculature
A child with VSD presents with development of cyanosis Left to right shunt, pulmonary hypertension, right
because of Eisemenger syndrome. correct sequence ventricular hypertrophy, right to left shunt
Child with perimembraneous VSD with CCF gets better Spontaneous closure
due to
Natural course of events in untreated ventricular septal Spontaneous closure, Sub acute bacterial endocarditis,
defects A normal life without symptoms

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CARDIOVASCULAR SYSTEM

X ray picture of VSD Dilated left atrium, Dilated pulmonary vein, Dilated
pulmonary arteries

PATENT DUCTUS ARTERIOSUS

Ductus arteriosus May cause machinery murmur by its patency

Ligamentum arteriosus is a remnant of Ductus arteriosus
th
Anatomical closure of ductus arteriosus 10 day
Complete Obliteration of Ductus arteriosus 6-12 days
Heart disease commonly associated with rubella PDA
infection
NOT a cyanotic heart disease PDA
PDA is more common in Females
Child with PDA Bounding pulses, pulmonary hemorrhage, necrotizing
enterocolitis
Differential Cyanosis PDA
Ductus arteriosus May cause machinery murmur by its patency
MC cause of death in adult with PDA CCF and infective endocarditis
Most important complication of PDA in child Cardiac failure
Least likely finding in PDA CO2 washout
Features of PDA Tachycardia
Most appropriate management for maintaining patency Prostaglandin E1
of ductus arteriosus in a neonate
Drug for Maintenance of Patency of PDA Alprostadil, Misoprostol
Closure of patent ducuts arteriosus stimulated by Prostaglandin inhibitors
Management of PDA in term child Indomethacin is not useful, surgery is
indicated
Gianturo coil PDA
PDA needs surgery to prevent development of Bacterial endocarditis
Contraindication of surgery in PDA Reversal of shunt

TRICUSPID ATRESIA

Congenital cyanotic heart disease with pulmonary Tricuspid atresia

oligemia
A patient presents with LVH and pulmonary Tricuspid atresia
complications, left axis deviation. most likely diagnosis
Central Cyanosis, Left Ventricular Hypertrophy, Left axis Tricuspid atresia
deviation
LVH, pulmonary complication.ECG shows left axis Tricuspid atresia
deviation
Central cyanosis with enlarged left ventricle Tricuspid atresia
Ebstein anomaly associated with Tricuspid atresia
Ebstein anomaly is associated with Pleural effusion, pericardial effusion,
ascites
Himalayan P wave is associated with Ebstein anomaly
Globular cardiomegaly with oligemic lung Ebstein anomaly

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CARDIOVASCULAR SYSTEM

fields
Tricuspid atresia Left axis deviation, Right ventricular hypoplasia,
Diminished pulmonary vascularity
Left ventricular hypertrophy and central cyanosis Tricuspid atresia
Great Box Shaped Heart Tricuspid Atresia
Plethoric lung field NOT seen in Ebstein anomaly
Intracavitatory echocardiography is a diagnostic aid in Ebstein anomaly of tricuspid valve
Surgeries for tricuspid atresia Fontann surgery, Glenn shunt

COARCTATION OF AORTA

Rib notching is produced by Coarctation of aorta, Neurofibromatosis, SVC

obstruction
Coarctation of aorta Systolic murmur across anterior chest and back and a
high pitched audible diastolic murmur in left sternal
border, Persistent hypertension despite complete
surgical repair
MC Site of Coarctation of Aorta Distal to Origin of Left Subclavian artery
MC condition associated with Coarctation of Aorta Bicuspid Aortic Valve
Coarctation of aorta associated with Bicuspid aortic valve, Turner syndrome, PDA
Shone Complex Coarctation of aorta, Left Sided Heart Lesions
Coarctation of aorta common in Turner’s syndrome
15 year old girl Short stature, Webbed neck, Sexual Turner’s Syndrome
infantilism, Coarctation of Aorta
Ribnotching of 4-9 ribs with double bulging Coarctation of aorta
Child presenting with headache, dizziness, intermittent Coarctation of aorta
claudication, occasional dyspnea
1 month old boy, failure to thrive, feature of congestive Coarctation of aorta
cardiac failure, femoral pulses are feeble compared to
brachial pulses
10 year boy, seizures, BP in upper extremity 200/140 Coarctation of aorta
mm Hg, femoral pulses NOT palpable
A child with 4 weeks of birth acyanotic, ejection systolic Coarctation of aorta
murmur is detected. causes are
Ejection Systolic murmur, Acyanotic child Coarctation
Intermittent claudication, dizziness, headache, likely Coarctation of aorta
lesion
Femoral pulse weak compared to radial and carotid Coarctation of aorta
pulse
Tortuous bronchial arteries Coarctation of Aorta
MC extracardiac abnormality associated with Notching of 1st and 2nd vertebra
coarctation of aorta
Dock’s sign (Inferior Rib Notching), ‘3’ Sign, ‘E’ Sign Coarctation of Aorta
Reverse 3 sign Coarctation of aorta
Collateral in post ductal coarctation formed from Suprascapular artery, Subscapular artery/internal
thoracic, Axillary artery
In post ductal coarctation of aorta blood supply to Vertebral artery, superior epigastric artery
lower limb NOT maintained through
Collateral in post ductal coarctation NOT formed from Vertebral artery
Cause of death in coarctation of aorta Infective endocarditis, CCF, Intracranial hemorrhage

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CARDIOVASCULAR SYSTEM

NOT a cause of death on coarctation Anterior MI

NOT a characteristic of Infantile coarctation Diastolic murmur is audible
Coarctation of aorta NOT associated with Renal artery stenosis, pulmonary stenosis
NOT true about coarctation of aorta Inability to augment cardiac output with exercise
Coarctation of aorta best diagnosed by MRI
Valvuloplasty NOT done in Coarctation of aorta

TOTAL ANOMALOUS PULMONARY VENOUS CONNECTION

Total anomalous pulmonary connection Total pulmonary venous flow reaches right atrium,
oxygen saturation of blood in the pulmonary artery is
higher than that in aorta, infracardiac type is always
obstructive
TAPVC All pulmonary veins enter by single trunk, Need not
always be associated with septal defects, Cyanotic heart
disease
MC Type of TAPVC Supracardiac
Snowman Sign, Figure of 8 sign, Cottage Leaf Sign, TAPVC (Supracardiac)
Double Contour
Groundglass Appearance, Edematous Septal line A>B TAPVC (Infradiaphragmatic/Obstructive)

TRANSPOSITION OF GREAT VESSELS

Infant of diabetic mother has Transposition of great vessels

Transposition of great arteries is common in Males
d-TGA Aortic valve is to the right of pulmonary artery, Right
ventricular pressure is elevated, A balloon arterial
septostomy should be performed to improve systemic
oxygenation
ECHO of a cyanotic 2 day old infant suggests right Transposition of Great vessels
ventricular enlargement
5 day old, full term male, severely cyanotic at birth, Transposition of great vessels
prostaglandin E was initially administered and lateral
ballooned atrial septostomy done, improvement in
oxidation
7 day old baby presented in the emergency department TGA
with unconsciousness, blue in appearance with 85% in
oxygen saturation
Neonate central cyanosis, short systolic murmur 2nd Transposition of great vessels
day of birth
Long Smooth curve to left border Physiologically Corrected TGA (L loop Transposition)
Egg on Side/Egg on String appearance Uncorrected TGA (d- TGA)
Surgery is always indicated in Transposition of great arteries
Rastelli procedure for TGA
Mustards Procedure TGA
Definite treatment of TGA Arterial switch
Surgeries for TGA Jatenus, Mustard, Senning, Rashkind

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CARDIOVASCULAR SYSTEM

EISENMENGER SYNDROME

Eisenmenger syndrome Pulmonary veins NOT distended, Pruning of peripheral

pulmonary arteries, Dilatation of central pulmonary
arteries
Eisenmenger complex is complex in adult in VSD, ASD, PDA
Signs of impending Eisenmenger syndrome Single S2, Increased intensity of P2, Graham Steel
murmur
Worst prognosis in Pregnant woman Eisenmenger syndrome
Heart disease having highest mortality in pregnancy Eisenmenger syndrome
Maternal mortality is highest in Eisenmenger syndrome
Tardive cyanosis Eisenmenger syndrome
Heath Edwards classification for Severity of Eisenmenger syndrome
NOT a feature of Eisenmenger syndrome LVH
NOT a feature of Eisenmenger syndrome Return of left ventricle and right ventricle to normal size
NOT true about eisenmenger syndrome RV and LV valve come back to normal size
NOT an indication of caesarean section in pregnancy Eisenmenger syndrome

HEART FAILURE

FEATURES OF HEART FAILURE

Cardiotoxic drugs Adriamycin, 5-FU, cyclophosphamide

Features of cardiac failure on patient with doxorubicin Anthracycline induced cardiac risk
Anthracyclines cause Vacuolar degeneration, myocyte loss
MC cause of Heart Failure in Infants Myocarditis
MC cause of Right Heart Failure Left Heart Failure
Pure right heart failure is due to Cor pulmonale
MC cause of heart failure in infancy Congenital heart disease
MC cause of congestive cardiac failure in infancy Congenital heart disease
Chief danger in children with paroxysmal atrial CCF
tachycardia
st
Earliest cause of CHF in 1 week of life Pulmonary atresia
NOT a precipitating cause of heart failure Polycythemia
Congestive heart failure triad Tachycardia, tachypnea, tender hepatomegaly
Heart failure cells are seen in Lung
Heart failure cells are seen in Chronic venous congestion of lung
Heart failure cells contain Hemosiderin
Nutmeg pattern of Liver Right sided heart failure
CCF is associated with increase in Right atrial mean pressure, serum urea, serum
norepinephrine
CCF associated with increase in Urea, right atrial mean pressure, nor epinephrine
Pure right sided heart failure is seen in Cor pulmonale
Pure left sided failure Aortic stenosis, Patent ductus arteriosus
MC cause of LVH Hypertension
Orthopnea in heart failure due to Reservoir function of leg veins

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CARDIOVASCULAR SYSTEM

Peribronchial edema in the setting of CCF Cardiac asthma

Congestive cardiac failure in infants is diagnosed by Liver enlargement
Congestive heart failure in children is best assessed by Tachycardia, Tender hepatomegaly
Uncommon finding in CCF in newborn Pedal edema
Grade I edema Pitting up to ankle
Idiopathic edema of women NOT related to menstrual cycle, increased water
retention in upright position, ACE inhibitors useful in
some cases
Uncommon finding in congestive cardiac failure in Pedal edema
newborn
Patients having acute cardiac failure do not show Fall in systemic capillary hydrostatic pressure
edema because
NOT a characteristic feature of Right sided heart failure Pulmonary edema
NOT a feature of right sided heart failure Increased PCWP
CCF NOT associated with increase in Sodium
NOT a characteristic of right sided failure Pulmonary edema
NOT a Framingham major criteria for diagnosis of heart Hepatomegaly
failure
NADA criteria Assessment of child for presence of heart disease
Pulmonary edema in CHF is due to Decreased plasma oncotic pressure
Congestive cardiac failure Kerley B lines, Pleural effusion, Cardiomegaly
Kerley B lines are seen if pulmonary pressure 25 mm Hg
Diagnosis of CCF in Infants Hepatomegaly
Paroxysmal atrial tachycardia may be terminated with Vasopressors, Valsalva manoeuve, Digitalis, Eye ball
pressure

DIAGNOSIS OF HEART FAILURE

Chest X ray finding in CCF Cardiomegaly, Thick interlobar septum

Feature of CCF Serum B type BNP is elevated
NOT a radiological feature of left ventricular heart Oligemic lung field
failure

MANAGEMENT OF HEART FAILURE

Drugs used in CHF Nesiritide, Digoxin, Spironolactone, Losartan

Digoxin used in CHF due to Atrial fibrillation and high ventricular rate
Most important pharmacological action of digoxin in Increase in ventricular contractile force
congestive cardiac failure
Drug of choice for congestive heart failure with ACE Inhibitors
hypertension
Inotropic drug Dopamine, amrinone, isoprenaline
Best inotrope agent to use in right heart failure Milrinone
secondary to pulmonary hypertension
Best ionotrope for use in right heart failure Milrinone
Drug that can be administered in LVF Morphine
Calcium channel sensitizer approved for use of CCF Levosimenden
In heart failure, which of these drugs sensitizes Levosimendan

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CARDIOVASCULAR SYSTEM

tropomyosin towards calcium

BNP is degraded by Neutral endopeptidase
Aminopeptidase inhibitors Bestatin, Apstatin
Niseritide Brain natriuretic peptide analogue
Niseritide Used in acutely decompensated heart failure, short half
life
Niseritide BNP analogue, Used in decompensated CHF, IV, Causes
loss of Na+ in urine
NOT true about niseritide Given orally
ANP analogue Caperitide, uralitide
In Alternative Medicine, used for Heart Failure Terminalia Arjuna
Drug NOT prolonging survival in chronic congestive Digoxin
cardiac failure
Drug avoided in elderly Digoxin in CCF
Drugs NOT used in CHF Nitroglycerine
NOT used in CHF Clopidogrel
Beta blockers NOT indicated in Acute CHF
Beta blocker in heart failure Absolutely contraindicated in acute decompensated
heart failure, Initiated at very low dose, Slow upward
titration of dose is required, Carvedilol most widely
used in this condition
NOT true about beta blocker therapy in congestive It should be started in optimum doses
heart failure
NOT true about use of beta blockers in heart failure Most effective in new onset decompensated heart
failure
NOT used for treatment of congestive heart failure Trimetazidine
Calcium channel blocker NOT used in Congestive heart failure
NOT used in congestive cardiac failure Trimetazidine
Medication NOT used in management of CCF in Soda bicarbonate
congenital heart disease
Ivabradine is used to Reduce heart rate
Istaroxime Na+ K+ ATPase inhibitor
Management of heart failure Biventricular pacing (also known as cardiac
resynchronization therapy)

CARDIAC GLYCOSIDE

DIGOXIN

Digoxin useful in Complete heart block with CHF

Digoxin NOT indicated in High output failure
Children does NOT tolerate better Digoxin
Digoxin is contraindicated in HOCM
Contraindication for digitalis Acute rheumatic carditis, Thyrotoxicosis, WPW
syndrome
Oubain acts by inhibiting Na+K+ ATPase
Positive inotropic effect of digitalis is due to inhibition Increased intracellular Na+ causing increased efflux of

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CARDIOVASCULAR SYSTEM

of Na+/K+ ATPase pump in cardiac muscle cell Na+ and increased influx of Ca++ through Na+/Ca+
membrane leading to exchanger in sarcolemma
Digitalis has positive inotropic effect by virtue of its Na+ K+ ATP ase pump
effect on
Decreases AV conduction Digoxin
Biochemical mechanism of digitalis is associated with Decrease in calcium uptake by sarcoplasmic reticulum
Mechanism of action of digoxin is Increase in systolic intracellular calcium
associated with levels
Digoxin Oral dose more than parenteral dose, Onset of action 6
hours, T half 48 hours, Preterm child needs more than
term
Digoxin 70-80% protein bound
Digitalis 95% protein bound
Drug deposited in muscle Digoxin
Digitalis Excretion is mainly renal, oral absorption is good, lipid
soluble
Digoxin is eliminated from body by Glomerular filtration
Digoxin can accumulate in toxic levels in patients with Renal failure
Digoxin action NOT affected in Hepatic disease
Compared to oral digitalizing dose, parenteral 2/3
digitalizing dose should be
Dose of digoxin in child as mg/kg 0.04 – 0.06
Time taken for digitalization 5 days
Dose of IV digoxin 0.25 mg
Dose of digoxin orally In adult 0.05 – 0.1 mg/kg
Therapeutic level of digoxin in 0.8 to 1.5 ng/ml
Toxic level of digitalis >2.4 ng/ml
Significant drug interaction with digoxin Cholestyramine, Thiazide diuretic, Quinidine
Dose of digoxin reduced when given with Quinidine, verapamil, calcium

DIGITOXIN

Does NOT contribute to digitoxin toxicity Hyponatremia

FEATURES OF DIGITALIS TOXICITY

Thiazide induced hypokalemia Increases digitoxicity

Digoxin toxicity enhanced by Hypokalemia, Quinidine, Hypomagnesemia,
hypothyroidism
Digoxin toxicity precipitated by Hypokalemia, hypomagnesemia, hypothyroidism
Digoxin toxicity aggravated by Hypokalemia, Hypercalcemia
Digoxin toxicity NOT enhanced by Hyperkalemia
ECG findings of digitalis toxicity Bigeminy, Junctional tachycardia, atrial tachycardia with
variable block
QT interval shortened in Digitalis toxicity
Most characteristic arrhythmia with digitoxicity PAT with block
Features of digitoxicity PAT with block, xanthopsia
AV block with atrial tachycardia is seen in Digitalis toxicity with K+ depletion

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CARDIOVASCULAR SYSTEM

Digoxin Paroxysmal AV tachycardia with AV block

Digoxin induced arrhythmia Paroxysmal atrial tachycardia with variable AV block,
ventricular bigeminy, may be used to treat AF
Rhythm disturbance characteristic of digitalis Paroxysmal atrial tachycardia
Drug producing emesis by acting centrally and Digitalis
peripherally
Digitalis induced arrhythmia is due to Increased trigger activity
Digitalis Toxicity causes Hyperkalemia
Digoxin produces SA block, AV block, hyperkalemia
Mitral regurgitation and atrial fibrillation presents with Digitalis toxicity
syncope. on examination person has a heart rate of
55.most probable cause
Chronic atrial fibrillation, regular heart rate Digitalis toxicity
Appearance of VT with the use of quinidine in Digitalis
treatment of atrial fibrillation is usually prevented by
prior administration of
60 year old man with rheumatic mitral stenosis with Digoxin
atrial fibrillation is on therapy for fast ventricular rate.
on treatment he developed regular pulse
NOT seen in digitalis toxicity Paroxysmal atrial tachycardia with fast ventricular rate

MANAGEMENT OF DIGITALIS TOXICITY

Digibind Treat digoxin toxicity

Best treatment of digitalis toxicity Fab fragments of digitalis antibodies
NOT a treatment of digitalis toxicity Hemodialysis
NOT indicated in digitalis toxicity Dialysis
NOT used in treatment of digitalis toxicity Hemodialysis
NOT a treatment of digitalis induced arrhythmia Calcium gluconate
NOT given in Digitalis toxicity Quinidine

VALVULAR HEART DISEASE

GENERAL FEATURES OF VALVULAR DISEASES

Typical movement of mitral valve Side to side

calcification
Lambl excrescences are seen in Aortic valve
Fluoroscopy is used in diagnosis Left ventricular function, Valve calcification,
Diaphragmatic palsy
Contraindication for mitral valvuloplasty Heavy calcification of mitral valve

MITRAL STENOSIS

Area of mitral orifice in adults 4-6 cm2

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CARDIOVASCULAR SYSTEM

Lutembacher syndrome Ostium secundum with Mitral stenosis

Parachute mitral valve Congenital mitral stenosis
Mimic physiological sign of Mitral stenosis Left atrial myxoma
MC heart disease associated with pregnancy Mitral stenosis
First symptom of mitral stenosis Dyspnea
Hemoptysis in Mitral stenosis High pulmonary artery pressure
Mitral stenosis is associated with Right ventricular hypertrophy
Typical movement of mitral calcification Upwards and downwards
th
Mitral stenosis cause Congestive heart failure in 30 week
pregnancy during
Mid diastolic murmur with presystolic accentuation Mitral stenosis
Fishmouth valve is seen in Mitral stenosis
Second stenosis in mitral stenosis Pulmonary arterial constriction
Left ventricular end diastolic is NOT common elevated Early mitral stenosis
in
NOT a feature of Mitral stenosis Obliteration of retrosternal shadow on lateral X ray
Severity of mitral stenosis is best assessed by LA enlargement, loudness of S1, Loudness of opening
snap
Severity of mitral stenosis assessed by Length of murmur
Severity of mitral stenosis S2-OS gap, prolonged diastolic murmur
NOT indicate severity of MS Opening snap delayed from S2
NOT true about severe MS Delay of opening snap
Double atrium, Lifting of left bronchus, Straightening of Mitral stenosis
left heart border, Posterior displacement of esophagus
Radiological features of mitral stenosis Double contour of right heart border, Straightening of
left heart border, Splaying of carinal angle, Kerley lines
Lifting up of left bronchus, Posterior displacement of
esophagus on barium swallow, Pulmonary
hemosiderosis, Straight left border of heart
X ray finding of mitral stenosis Lifting up of left bronchus, double atrial shadow,
posterior displacement of oesophagus on barium
swallow
Inverted moustache sign Mitral stenosis
Ideal time for surgery for Mitral stenosis 14 weeks
Balloon valvotomy is NOT successful in Calcified mitral stenosis
Mitral balloon valvuloplasty is NOT indicated in Calcified Mitral valve
NOT indicated in mitral stenosis in pregnancy Methergine at delivery of anterior shoulder

MITRAL REGURGITATION

Earliest valvular lesion in case of acute rheumatic fever Mitral regurgitation

Commonest rheumatic valvular disease Mitral regurgitation
MC Rheumatic Valvular Disease Mitral Regurgitation
Cause of Mitral Regurgitation Myxomatous degeneration
Myxomatous degeneration is associated Mid systolic click
with
Common valvular lesion in myocardial infarction Mitral regurgitation
Nocturnal angina pain, severe diaphoresis Chronic severe MR
18 year girl, rheumatic carditis, mitral insufficiency Decreased functional residual capacity

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CARDIOVASCULAR SYSTEM

Murmur in mitral regurgitation Pan systolic murmur

Valsalva increases pansystolic murmur of Mitral regurgitation
Severity of mitral regurgitation decided by Presence of diastolic murmur across mitral valve, wide
split second heart sound, presence of left ventricular S3
gallop
Severity of mitral regurgitation judged by Left ventricular S3
Severity of mitral regurgitation is NOT decided by Intensity of systolic murmur across mitral valve
59 year old woman, severe myxomatous mitral Mitral valve repair or replacement
regurgitation is asymptomatic with left ventricular
ejection fraction of 45% and an end systolic diameter
index of 2.9 cm/m2. most appropriate treatment is

MITRAL VALVE PROLAPSE

In mitral valve prolapse syndrome, mitral valve HPE Myxomatous degeneration

shows
Mitral valve prolapse Autosomal dominant, myxomatous degeneration in
valve leaflets, asymptomatic, common cardiovascular
manifestation of Marfan’s syndrome
Mitral valve prolapse Common in females, benign clinical course, transient
cerebral ischemia is a known complication
Young patient, systolic murmur at apex, murmur MVP
increases on both handgrip and valsalva maneuver
Auscultatory findings of Mitral valve prolapse Mid systolic click, late systolic murmur, non ejection
click
Midsystolic click in asymptomatic young female Mitral valve prolapse
Complications of mitral valve prolapse Mitral regurgitation, arrhythmia, sudden
death, transient ischemic attack, infective
endocarditis
Asymptomatic young woman, systolic murmur Echocardiography
arrhythmia, mid systolic click

AORTIC STENOSIS

Complication of Hypervitaminosis D Supravalvular Aortic stenosis

Supravalvular aortic stenosis William’s syndrome
Heyde syndrome Aortic stenosis with GI bleeding
NOT a common manifestation of congenital rubella Aortic stenosis
Angina pectoris and syncope most likely to be Aortic stenosis
associated with
Angina, syncope, congestive heart failure Aortic stenosis
Physical sign in patient with severe aortic stenosis Delayed peak of systolic murmur
Supravalvular aortic stenosis is associated with Absence of ejection click, Concentric hypertrophy of left
ventricle, Aortic regurgitation murmur
Pressure difference of 5 mm Hg between two upper Supravalvular aortic stenosis
limbs in
Pressure volume curve is shifted to left in Aortic stenosis
Sustained heaving cardiac impulse Aortic stenosis

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CARDIOVASCULAR SYSTEM

Calcification of aortic valve Aortic stenosis

Gallavardin effect Coarse systolic murmur of AS, sound high pitched and pure
at apex
Gallavardin phenomenon Seen in aortic stenosis, murmur is misinterpreted as mitral
regurgitation
Angina pectoris is common with AS
MC cause of death in aortic stenosis in children Ischemic heart disease with ventricular fibrillation
Paradoxically split second heart sound signifies Severe AS
Severe aortic stenosis ST and T wave changes
Exercise testing is absolutely contraindicated in Aortic stenosis
Vasopressor of Choice in Aortic Stenosis Phenylephrine
Ross procedure for Aortic stenosis
Surgeries for congenital aortic stenosis Ross, Konno

AORTIC REGURGITATION

Diastolic mitral regurgitation Aortic regurgitation

Characteristically result in aortic valve Syphilitic heart disease
insufficiency
Aortic regurgitation seen in Marfan syndrome, bacterial endocarditis, ankylosing
spondylitis
Acute aortic regurgitation NOT seen in Acute MI
Young basket ball player, ht 188 cm arm span 197 cm, Aortic regurgitation
diastolic murmur best heard in 2nd right intercostals
space
Cardiac lesion having highest risk of occurrence of Valvular aortic regurgitation
infective endocarditis
Aortic regurgitation Collapsing pulse, Duroziez’s murmur, mid diastolic
murmur, LVH
LVH commonly seen in Aortic incompetence
Water hammer pulse Aortic regurgitation
Low pitched delayed Diastolic Murmur in Severe Austin Flint Murmur
Chronic AR
Hill sign More than 20 mm Hg difference in
popliteal and brachial systolic cuff
pressure
Blood pressure in severe aortic regurgitation 60-75 mm Hg
NOT a murmur in aortic regurgitation Pansystolic murmur

TRICUSPID REGURGITATION

MC cause of tricuspid regurgitation Secondary to dilatation of right ventricle

Commonest cardiac manifestation in carcinoid Tricuspid regurgitation
Essential for diagnosis of tricuspid regurgitation Systolic murmur in tricuspid area, pulsatile liver
Hepatomegaly and liver pulsation Tricuspid regurgitation
Enlarged pulsatile liver Tricuspid regurgitation
Carvallo sign Tricuspid regurgitation murmur increases with inspiration
Positive hepatojugular reflex Tricuspid regurgitation, PS, right heart failure, right

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ventricular infarction, pre capillary pulmonary

hypertension
Positive hepatojugular reflex NOT found in Decreased afterload

PULMONARY STENOSIS

MC form of isolated right ventricular obstruction Valvular pulmonary stenosis

MC type of pulmonary stenosis Valvular
Pulmonary stenosis is associated with Noonan syndrome, Alagille syndrome
Peripheral pulmonary stenosis is associated with William syndrome, Rubella
Rapidly progressing pulmonary stenosis Amiodarone poisoning
Obstruction in pulmonary stenosis Supravalvular, valvular, subvalvular
Obstruction in pulmonary stenosis may occur at Supravalvular, Valvular, Subvalvular
Cardiac abnormality well tolerated during fetal life, Pulmonary valve stenosis
serious problem at birth

ENDOCARDITIS

ETIOLOGY OF ENDOCARDITIS

HACEK Hemophilus, Actinobacillus, Cardiobacterium, Eikenella,

Kingella
HACEK group does NOT include Acinetobacter barumannii
MC cause of Acute bacterial Endocarditis Staphylococcus aureus
MC cause of endocarditis in IV drug users Staphylococcus aureus
MC cause of infective endocarditis in Congenital heart disease
pediatric age group
MC cause of tricuspid valve vegetation Staphylococcus aureus
Anti teichoic acid antibodies in Staphylococcus
endocarditis
Cause of infective endocarditis associated Pseudomonas aureginosa, serratia
with IV drug abusers
MC cause of infective endocarditis Coagulase negative staphylococci
associated with indwelling catheter
MC cause of Prosthetic Valve Endocarditis Staphylococcus epidermidis (Coagulase negative)
Serious prosthetic valve infection caused by Staphylococcus lugdunensis, S. schleiferi
MC cause of sub acute endocarditis α Hemolytic Streptococci (Viridans)
MC cause of native valve endocarditis Streptococcus viridians
MC cause of infective endocarditis Viridians streptococci
associated with dental procedures
MC cause of infective endocarditis Group D enterococci
associated with large bowel and
genitourinary manipulation
Cause of infective endocarditis associated Fungal

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with open heart surgery

Infective endocarditis in elderly with Streptococcus bovis
colonic polyp or cancer is associated with
Infective endocarditis due to pseudomonas is most Intravenous abuse of pentazocin
commonly seen in
Most common pathogen in culture negative endocarditis Coxiella burnetti, bartonella
Most common cause of endocarditis VSD
Least likely to cause infective endocarditis Salmonella typhi
Least common cause of endocarditis ASD
Acute infective endocarditis with abscess formation Staphylococci
A patient of RHD developed infective endocarditis after Streptococcus viridians
dental extraction. most likely organism
A 2 year old known case of RHD presents with 3 weeks Staphylococcal endocarditis
history of fever, hematuria and palpitation. diagnosis

SITE OF ENDOCARDITIS

Valve pocket vegetations are seen in Libman Sack endocarditis

Flat small reddish tan vegetations in the Libman sack endocarditis
cusps of tricuspid and mitral valve
MC Site of Vegetations in Libman Sack Endocarditis Mitral & Tricuspid Valve
MC Site of Non Bacterial Thrombotic Endocarditis Mitral>Aortic>Tricuspid
(Marantic Endocarditis)
MC affected valve in Prosthetic valve Endocarditis Aortic
Heart valve most likely to be involved in infective Tricuspid valve
endocarditis following septic abortion
MC heart valve involved in IV drug user Tricuspid

FEATURES OF ENDOCARDITIS

Most friable vegetation Infective endocarditis

Maximum destruction of valves Acute infective endocarditis
Site of lesion of endocarditis of RHD Along line of closure of valves
Endocarditis is commonest in MR
Immune complex lesions in SBE Osler’s nodes, Microscopic hematuria, Roth spot
Flat vegetations in pockets of valves are due to Libman sacks endocarditis
Vegetations on undersurface of AV valves are found in Libman sack’s endocarditis
Libman sack’s endocarditis Medium sized vegetations on both side of
valve leaflets
Vegetation in Libman Sach’s Endocarditis Sterile vegetation
Libman sack’s endocarditis SLE
Non bacterial thrombotic endocarditis is Terminal neoplastic diseases
commonly associated with
Not firmly fixed to valve Non bacterial thrombotic endocarditis
Woman having septic abortion done, vegetation on Septic infarcts to lung
tricuspid valve is likely to go to
Tricuspid valve endocarditis in septic abortion most Lungs

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likely affect
Osler’s nodes are typically seen in Acute staphylococcal endocarditis
Osler node seen at Tips of palms and soles
Roth spots seen in Infective endocarditis
Roth spots are due to Retinal hemorrhage
Roth spots (White central hemorrhage) may arise in Anemia
NOT included in Duke’s minor criteria Endocardial involvement
NOT a diagnostic criteria for infective endocarditis Raised ESR, Rheumatic factor
NOT true about infective endocarditis May lead to acute regurgitant valvular lesion
NOT a feature of infective endocarditis Thrombus in left atria
NOT a complication of infective endocarditis Suppurative pericarditis
NOT a complication of infective endocardits Myocardial infarction
Mitral valve vegetations do NOT embolise to Lung
Splenomegaly is more common in Sub acute endocarditis

MANAGEMENT OF ENDOCARDITIS

Antibiotic prophylaxis for infective endocarditis in Coarctation of aorta

Antibiotic prophylaxis for oral cavity procedures in Amoxycillin
infective endocarditis
Initial therapy for all HACEK except Eikenella Ceftriaxone
Therapy for Eikenella Ampicillin

PERICARDIAL DISEASES

GENERAL FEATURES OF PERICARDIUM

Most common non penetrating cardiac injury Myocardial contusion

Hemopericardium Ruptured aortic aneurysm, myocardial infarction, chest
injury
Pericardial friction rub heard frequently at End of Expiration

CARDIAC TAMPONADE

Engorged neck veins, BP 80/50 pulse rate 100 following Cardiac tamponade
blunt trauma to chest
Postoperative cardiac surgical patient developed Cardiac tamponade
sudden hypotension, rapid central venous pressue,
th
pulsus paradoxus in 4 postoperative hour
Carcinoma lung, respiratory distress, electrical alterans Cardiac tamponade
Diastolic collapse of right ventricle on echocardiogram Cardiac tamponade
Beck’s triad in Cardiac tamponade Muffled Heart Sounds/Silent Heart, Distended Neck
Veins, Hypotension
Beck’s triad seen in Cardiac tamponade

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Electric alterans is seen in Cardiac tamponade

Pulsus paradoxus is characteristic of Cardiac tamponade
Kussmaul sign is NOT seen in Cardiac tamponade
NOT a feature of Cardiac tamponade Warm periphery
Cardiac tamponade Low voltage ECG
Cardiac tamponade ABSENT y descent
Feature of JVP in cardiac tamponade Prominent x descent with absent y descent
Best investigation for Cardiac tamponade 2D echocardiography
In case of tamponade after trauma Pericardiocentesis at once may be life saving
Treatment of acute cardiac tamponade Emergency paracentesis

PERICARDITIS

Drugs associated with pericarditis Hydralasine, Procainamide, Methysergide, Emetine

Drugs causing pericarditis Methysergide, Hydralasine, Minoxidil
Emetine, Methysergide, Procainamide Pericarditis
Drug used in HIV causing pericarditis Didanosine
Cause of pericarditis Tuberculosis, Uremia, Rheumatic fever
MC cardiac manifestation of SLE Pericarditis
Pericarditis is always painful Pyoperitoneum
Typical feature of pericardial involvement on physical Friction rub
examination
In case of chest pain with pericarditis and pericardial Phrenic nerve
effusion, pain is referred by
Pain in pericarditis increases on Leaning forward
Pain of acute pericarditis is relieved by Sitting
NOT seen in pericarditis Pulsus paradoxus
ECG finding in acute pericarditis Global ST segment elevation in early pericarditis, sinus
tachycardia is common finding, PR segment depression
is present in majority of patients
Hemorrhagic pericarditis Transmural myocardial infarction, Dissecting aneurysm
of aorta, Metastatic disease of pericardium
Hemorrhagic pancreatitis does NOT occur in Constrictive pericarditis
Commonest cause of constrictive pericarditis in India Tuberculosis
Least likely to cause constrictive pericarditis Acute rheumatic fever
Chronic constrictive pericarditis Ascites is NOT in proportion to edema, Right ventricular
end diastolic pressure is raised
During ventricular pressure pulses, square root wave Constrictive pericarditis
sign
Constrictive pericarditis Ascites, Retractile apex, Pericardial knock
NOT a cause of ST elevation Constrictive pericarditis
ST elevation NOT seen in Constrictive pericarditis
Kussamaul sign Constrictive Pericarditis
Pericardial Calcification, thickened pericardium, Square Constrictive Pericarditis
root sign, Egg in cup appearance
Friedrich sign (rapid or exaggerated y Constrictive pericarditis
descent)
Broadbent sign Reduced apical impulse in chronic constrictive pericarditis
Definitive treatment of constrictive pericarditis Pericardial resection

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Water bottle configuration of heart Pericardial effusion

Water can appearance of chest X ray Pericardial effusion
Ewart’s sign Pericarditis with effusion
Ewart’s sign Cardiac tamponade
Best investigation for pericardial effusion ECHO
Investigation used to differentiate Pericardial effusion Echocardiogram
and Heart dilatation
Signs of pericardial effusion are difficult to detect 500 ml

HYPERTENSION

BLOOD PRESSURE

Immediate change after lying down Increased venous return

Mean circulatory filling pressure Arterial pressure taken at point when heart stops
beating
During diastole, arterial pressure is maintained by Elastic recoil of aorta
Positive pressure head in aorta during Elastic property of aorta
diastole is maintained by
Blood pressure Peripheral resistance * cardiac output
Blood pressure peripheral resistance * cardiac output
Blood pressure Cuff width should be 40% of arm circumference,
th
Diastolic blood pressure is indicated by 5 koratkoff
sound, Small cuff measures spuriously elevated diastolic
BP, Monkenberg sclerosis causes pseudohypertension
Blood pressure measurement Cuff width should be 40% of arm circumference, small
cuff measures spuriously elevated diastolic blood
pressure, monkenberg sclerosis causes
pseudohypertension
B.P measurement correct is 80% of circumference of a limb
SI unit of blood pressure KPa
Investigation of flight induced stress on blood pressure. Lying down position
BP twice measured. Once before takeoff and once after
space craft entered orbit. For proper comparison
preflight BP should be recorded in
Pressure required to occlude blood flow with a 25 – 50 mm Hg
tourniquet that exceeds systolic pressure
Blood pressure measured by sphygmomanometer Higher than intraarterial pressure
Sphygmomanometer blood pressure is More than interarterial pressure
Experiment for BP on dog. Rakesh uses Falsely low values at high pressure in pulse tracing
sphygmomanometer on right femoral artery. Arif
pressure transducer on left femoral artery. Mean
arterial pressure both 100 mm hg, 5 mins after
adrenaline . Rakesh 130.arif 120-
Spuriously high BP NOT seen in Ausculatatory gap
A blood pressure of 120/80 mm Hg is elevated for 4 years
children aged
Average BP of one year old child 95/50

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Systolic BP in stage 2 hypertension >160

Hypertension in children Greater than or equal to 95th percentile for
age, sex and height at 3 occasions
Least likely cause of secondary Wilm’s tumor
hypertension in pediatric age group
Most accurate non invasive method for Oscillometric method
measuring BP
Drug useful for hypotensive anaesthesia Trimethaphan
NOT used for induced hypotension during surgery Mephentermine

CAUSES OF HYPERTENSION

MC cause of Systemic Hypertension in Children Acute Glomerulonephritis

MC cause of Secondary Hypertension in Children Renal Disease
Acute onset of hypertension in children Acute Glomerulonephritis
Cause of Persistent hypertension in Children Renal Parenchymal Lesion
Monogenic autosomal dominant cause of hypertension Gordon syndrome, Pregnancy Exacerbated
hypertension, glucocorticoid remediable aldosteronism
Hypercarbia characterized by Hypertension
Hypersecretion of aldosterone causes Hypertension
Hypertension caused by Erythropoietin, cylclosporine, NSAID
Renovascular hypertension is aggravated by ACE inhibitors
NOT a cause of hypertension with hypokalemia End stage renal disease
Hypertension is NOT caused by high intake of Potassium

FEATURES OF HYPERTENSION

Rapidly evolving end organ damage is a feature of Hypertensive emergency

Hypertensive urgency Can be managed without extensive monitoring on an
outpatient basis
Accelerated hypertension associated with Metabolic alkalosis
Features of essential hypertension Concentric hypertrophy of LV, increased heart size,
increased size of heart muscles, myohypertrophy
Multifactorial disorder Systemic hypertension
J curve phenomenon is associated with Hypertension
Pseudo resistant hypertension occurs in Patients going to office

RENOVASCULAR HYPERTENSION

MC cause of Renovascular Hypertension in Young in Takayasu arteritis

India
MC cause of Renovascular Hypertension in young in Fibromuscular Dysplasia
western world
NOT a feature of renovascular hypertension Muscle cramps
Most specific and sensitive investigation in case of MRI
renovacular hypertension
Most sensitive and specific investigation for screening Spiral CT

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of renovascular hypertension
Renovascular hypertension Captopril

MORPHOLOGY OF HYPERTENSION

Monkenberg sclerosis Pseudohypertension

Calcification of tunica media is mostly related to Monckberg sclerosis
Monckeberg sclerosis involves Media
Monckeberg calcific sclerosis affects medium sized Media
arteries by involving structure of
Changes in heart in essential hypertension Cardiac cell hypertrophy
Pathological change in kidney in benign hypertension Hyaline arteriosclerosis
Hyaline arteriosclerosis is seen in Benign nephrosclerosis, Hypertension, Diabetes
NOT a feature of benign hypertension in kidney Fibrinoid necrosis
Characteristic pathologic feature of Malignant Fibrinoid Necrosis
hypertension
Characteristic feature of Kidney in Malignant Fibrinoid necrosis
hypertension
Pathological change in malignant hypertension Hyperplastic arteriosclerosis
Malignant hypertension is associated with Malignant nephrosclerosis
Hyperplastic arteriosclerosis is associated SLE
with
Onion skin thickening of arteriolar wall is seen in Hyperplastic arteriosclerosis
Hyperplastic arteriosclerosis in malignant hypertension Heart
is NOT seen in
Does NOT occur in malignant hypertension Hyaline arteriosclerosis

MANAGEMENT OF HYPERTENSION

Primary prevention of hypertension Weight reduction, exercise promotion, reduction of salt

intake
Management of uncomplicated essential hypertension Diet modification, exercise drugs
First line management of Hypertension in Diabetes ACE Inhibitors, ARB
Drug of choice In hypertension due to Phentolamine
pheochromocytoma
Antihypertensives having neutral role in lipid Losartan, Prazosin
metabolism
Antihypertensive devoid of central action Indapamide
Antihypertensive drug causing hypothyroidism Amiodarone
Antihypertensive NOT contraindicated in pregnancy Labetalol
Antihypertensive NOT used in type II diabetes Thiazides
NOT a preferred agent of hypertension in diabetes Hydrochlorthiazide
NOT used in severe hypertension on elderly on Prazosin
empirical basis
Combination NOT recommended for treatment of ACE inhibitors and Beta blockers
hypertension
NOT true about hypertension In hypertensive patients with gout, diuretics are
preferred

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Antihypertensives to stopped before Surgery ACE Inhibitors, ARB

Diazoxide cause Hyperglycemia
True about vasomotor centre Acts along with cardiovagal centre to maintain blood
pressure
Methyldopa, Clonidine acts on Vasomotor centre
Postural hypotension is common with Prazosin

VASODILATORS

Vasodilators NO, CO2, N2O, CO, Helium

Drug causing peripheral vasodilatation by direct action Minoxidil
which is useful where other therapy is inadequate or
where severe hypertension is present
Minoxidil is a Antihypertensive
Only vasodilator that can be inactivated Vasoactive intestinal peptide
by proteolytic enzymes
Side effects of directly acting vasodilators Hypertrichosis, Hypotension

ARTERIOLAR DILATORS

Arteriolar dilators Hydralazine, Nifedipine, Prazosin, Enalapril

Hydralazine Direct relaxation of arterioles, postural hypotension is
NOT common, increases plasma rennin activity
Hydralazine Predominant arterial dilator
NOT an predominant arteriolar dilator Sodium nitroprusside

VENOUS DILATORS

Venodilator Nitroprusside
Mechanism of action of sodium nitroprusside Stimulation of guanylate cyclase
Side effects of sodium nitroprusside Lactic acidosis, Psychosis, Headache

ACE INHIBITORS

Action of angiotensin II Systemic vasoconstriction and retention of water

Angiotensin II does NOT cause Vasodilatation
ACE inhibitor and ARB Decrease total peripheral resistance
ACE inhibitors Omission of prior dose decreases risk of postural
hypotension
Antihypertensive of choice in diabetes and ACE inhibitors
microalbuminuria
ACE inhibitors NOT contraindicated in Diabetes
ACE inhibitors NOT useful in Pheochromocytoma
Most significant adverse effect of ACE inhibitor Hypotension
Long term use of ACE inhibitors cause Reduction in filtration fraction

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ACE inhibitors cause Persistent cough, Taste changes, First dose

hypotension, Angioedema
Antihypertensive causing renal failure ACE inhibitors
ACE inhibitors cause Hyperkalemia
Cough and angioedema in patients taking ACE inhibitor Bradykinin
due to
Maximum bicarbonate excretion is seen with ACE inhibitors
NOT an adverse effect of ACE inhibitors Hypokalemia
Captopril exerts antihypertensive effect by Inhibits conversion of angiotensin I and II
Drugs causing afterload reduction Captopril
Side effects of captopril Cough, Hyperkalemia, Renal dysfunction
Dysguesia is a side effect of Captopril
NOT used in pregnancy associated hypertension Captopril
Provides hemodynamic stability and prolong survival in Lisinopril
congestive heart failure
Side effects of Lisinopril Dizziness, Cough, Angioneurotic edema
ACE inhibitors are contraindicated in Bilateral renal artery stenosis, Renal failure, Elderly
Enalapril Prodrug, more effective than captopril, less adverse
effect, NOT a dipeptide
Enalapril Useful in heart failure, longer acting than captopril,
prodrug
Young patient 190/120 mm Hg, without any clinical Oral enalapril
symptom and normal fundus examination
ACE inhibitor whose bioavailability NOT affected by Enalapril
food
Antihypertensive agent can be used in gout with Enalapril
diabetes mellitus
Antihypertensive NOT used in pregnancy Enalapril
Antihypertensive Contraindicated in pregnancy Enalapril
Enalapril is contraindicated in Single kidney, bilateral renal artery stenosis,
hyperkalemia
Best for reducing proteinuria in diabetic patient Perindopril

ARB

ARB inhibitors Continued till the day of operation

Losartan Competitive angiotensin receptor antagonist, long
acting metabolite, associated with negligible cough
NOT true about losartan Cause hyperuricemia

CALCIUM CHANNEL BLOCKER

Calcium channel blocker used in treatment of Verapamil, Nifedipine

hypertension
When nitrates combined with calcium channel blockers Arterial pressure will decrease
Antihypertensive inhibiting labour Nifedipine
Antihypertensive causing gingival hyperplasia Nifedipine
Racemic mixture of two enantiomers with different Verapamil

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pharmacokinetic and pharmacodynamic property is

seen in
Maximum effect of contractility of heart Verapamil
Calcium channel blocker with maximum effect of Verapamil
conduction of heart is
ECG change caused by verapamil Increases PR interval
NOT a dihydropyridine Verapamil
Drug causing constipation Verapamil
Verapamil is carefully used in presence of Beta blockers
Propanolol should NOT be given to patient on Verapamil
treatment with
Combination of beta blockers and calcium channel Heart block, Bradycardia
blockers cause
Verapamil contraindicated in Complete heart block
NOT a calcium channel blocker Pirenzepine
NOT a ca channel blocker Dantrolene
Ion does NOT causing Vasodilatation Ca++
Does NOT significant drug interaction with digoxin Amlodipine
Calcium channel blocker NOT used in Sick sinus syndrome
Side effect of calcium channel blocker Gingival overgrowth
Antidote for calcium channel blocker overdose Calcium gluconate

BETA BLOCKERS

First line drug for management of hypertension in Beta blocker

patients with angina
Anti hypertensive agent associated with maximum Beta blockers
incidence of impotence
Drug NOT used in Hypertensive patient with Glaucoma Beta blockers
Drug contraindicated in hypertensive cardiac failure Atenolol
Antihypertensive causing decreased libido and Atenolol
impotence
NOT a frontline antihypertensive agent Atenolol
NOT used to reduce afterload Propanolol

CLONIDINE

Clonidine Alpha adrenergic agonist, Dry mouth as adverse effect,

Inhibits sympathetic flow, Prazosin does NOT
completely antagonize its action
Clonidine Increases parasympathomimetic outflow, decreases
sympathetic outflow by blocking central alpha receptor,
used in hypertension
Clonidine Alpha 2 selective agonist
Clonidine Reduction in central sympathetic outflow, combined
with vasodilators, sedation and xerostomia are common
side effects
Antihypertensive causing sedation Clonidine
Sudden withdrawal of which drug result in serious Clonidine

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adverse cardiovascular changes in patient taking the

drug over long time
NOT true about clonidine Increase in LDL cholesterol on prolonged usage
Clonidine withdrawal Hypertension Phentolamine, Tolazoline

METHYLDOPA

Methyldopa acts by Altering central sympathetic nervous activity

Methyldopa primarily used in Pregnancy induced hypertension
Antihypertensive agent decreasing libido Methyldopa
Warm antibody type of hemolytic anemia associated Methyldopa
with

MANAGEMENT OF HYPERTENSIVE EMERGENCY AND URGENCY

Hypertensive crisis is pheochromocytoma caused by Propanolol, saralasin, captopril

Rapid reduction of blood pressure indicated in Acute aortic dissection, hypertensive encephalopathy,
intracerebral hemorrhage
Drug of choice in hypertensive emergency Sodium nitroprusside IV
Drug of choice for malignant hypertension in 6 year old Sodium nitroprusside
child
Sodium nitroprusside Increased guanylate cyclase
Sodium nitroprusside infusion may result in Cyanide toxicity
To prevent toxic accumulation of cyanide during rapid IV sodium thiosulphate
infusion of sodium nitroprusside ,best drug to be given
Fenoldopam is used in Hypertensive emergencies
Drug used in hypertensive crisis Diazoxide
Hypertensive Emergency in pregnancy Hydralazine
Treatment of hypertensive crisis in patient with Nifedipine, clonidine
autonomic dysreflexia
NOT used for hypertensive crisis Indapamide, clonidine, phenoxybenzamine, methyldopa
Inappropriate choice of pharmacological management Nifedipine
in hypertensive emergency
Grade II hypertensive retinopathy with BP 230/110 mm Sublingual nifedipine
Hg. NOT a treatment
NOT an IV therapy for hypertensive emergencies Nifedipine

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