AGT notes

AGT’s Notes
compiled by
Dr. Pawan Kumar

AGT’s Notes compiled by Dr. Pawan Kumar
AGT’s Notes Compiled by Dr. Pawan Kumar 2
INDEX
Page No.
1) Anatomy 02
2) Physiology 06
3) Proforma for cardiac case 09
4) Cardiopulmonary bypass 55
5) Valvular heart disease 70
6) Surgery for valvular heart disease 87
7) Congenital acyanotic heart disease 103
8) Congenital cyanotic heart disease 132
9) Cardiac catheterization 166
10)Coronary artery disease 171
11)Constriction & cardiac tumors 186
12)Aorta, lung & mediastinum 189
13)Trauma & CPR 204
14)X-Rays 206
15)Vascular 208
16)Drugs & First’s 214
17)Instruments 223
18)Surgeons 240
19)Journals 245

ANATOMY
Q-Where is the term ‘cardiac’ derived from?
A-In Greek ‘Kardia’ means ‘Heart’.
Q-What is the long axis of the heart?
A-It runs from the right shoulder to the left hypochondrium.
Q-What is distribution of cardiac mass with respect to midline?
A-1/3rd of the cardiac mass lies on the right & 2/3rd on the left.
Q-When is a vessel termed as an arteriole or capillaries?
A-When diameter is 0.3mm and just visible to the naked eye they are called arterioles.
Capillaries are ½ - 1 mm in length and 7μm diameter allowing RBC’s to pass in a single
file.
Q-Describe the anatomy of bony thorax.
A-Upper 6 ribs join with the vertebrae posteriorly & the sternum anteriorly.
Ribs 7 – 10 articulate with the vertebral elements posteriorly and then fuse their anterior
costal cartilage into the flexible costal margin.
11th and 12th ribs articulate with thoracic vertebrae but are unattached anteriorly. They are
referred to as floating ribs.
Q-What is the direction of intercostal muscle?
A-It is as follows:
Muscle Direction
External: Hands in front pocket
Internal: Hands in back pocket
Transversus thoracis: Irregular
Q-Describe the anatomy of intercostal arteries.
A-
Anterior ICA: The Anterior ICA and vein arise from the ITA.
Posterior ICA: arise from descending thoracic aorta – 3 – 12 in number. The first two
posterior ICA arise from the costocervical trunk. Post IC Veins drain into the azygous
and hemiazygous respectively
Post ICA bifurcates into 2.
Ant and post ICA anastomose near the mid clavicular line
The internal mammary artery lies between the sternum and the transverses thoracis.
Q-Describe the surface anatomy of valves.
A-It is as follows:
All the 4 valves lie posterior to the sternum on an oblique line joining the 3rd left
sternocostal joint with the 6th right sternocostal joint.

Site of auscultation:
Pulmonary: left 2nd ICS just left of the sternum
Aortic: Right 2nd ICS just right of the sternum
Mitral: apex (5th ICS)
Tricuspid: 5th ICS on the right of the sternum
Q-Describe the nerve supply of heart.
A-It is as follows:
Sympathetic – cervical sympathetic ganglia & the upper thoracic sympathetic trunk.
Parasympathetic- From the Vagus-single cervical branch in neck, 1-2 cervicothoracic
branches at inlet and 2-4 thoracic cardiac branches from main branch in thorax. Right
vagus supplies the SA node while the left vagus supplies the AV node.
Q-Describe briefly the embryology of heart.
A-
-3rd week- fusion of 2 endocardial tubes forms the primitive heart.
-The muscular wall of this to be begins to contract, caudal to cranial
-5 sacculations develop, viz., sinus venosus, atrium, ventricle, bulbous cordis & truncus
arteriosus.
-Constriction between the atria & the ventricle becomes the AV/ coronary sulcus
-The paired vessels projecting cranially from the truncus arteriosus, arch posteriorly to
form the dorsal aorta, are the first aortic arches
-Also the heart is suspended from the posterior wall of the embryo in a dorsal
mesocardium
-Extensive growth of the heart, relative to the surroundings thoracic structure, causes the
primitive heart tube to undergo folding into an ‘S’ shape.
-The venous portion of the heart (cardinal veins, sinus venosus & primitive atrium) form
the base of the heart, while the primitive ventricle projects anteriorly into the pericardial
cavity & the ascending truncus arteriosus exits the pericardial sac superiorly.
Fate of dorsal mesocardium- the breakdown of the dorsal mesocardium between the
arterial end (bulbous cordis & venous end of primitive atrium) results in the formation of
the transverse pericardial sinus. This is the adult heart is demonstrated between the great
arteries & the great veins
Formation of 4 Chambered heart-4th week of development the partitioning of the
primitive heart into 4 chambers begin. Each of the primitive atrium & ventricles begin to
separate by saggittal ingrowths, the atrioventricular endocardial cushions. .
Their fusion during 5th week results in a partitioned 2-chamber heart with 2 AV canals
communicating between the atria & ventricles.
Formation of aorta & PA- 5th week a spiral septum forms in the truncus & descends in a
clockwise fashion to separated into 2 tubes.

Q-Define Mediastinum & its describe its divisions?
A-
Def. of mediastinum- A septum that divides the thoracic cavity & contains all thoracic
viscera, except the lung’s. It extends from posterior aspect of sternum to the bodies of
vertebrae & from thoracic inlet superiorly to the diaphragm inferiorly.
It is divided by an imaginary line thru’ the sternal angle to T4 / T5 space, the
mediastinum is divided into superior & inferior.
Inferior is further divided into anterior, middle & posterior.
Q-What are the contents of the Mediastinum?
A-The contents are:
Superior Mediastinum:
1. Retrosternal structures.
- Thymus
- Great veins.
2. Prevertebral
- Trachea
- Esophagus
- Lt. recurrent laryngeal nerve
- Thoracic duct
3. Intermediate
- Vagus n
- Phrenic n
- Aortic arch & 3 branches
Q-What thoracic structure is not included in the mediastinum?
A-Lungs.
Q-What is the fate of aortic arches?
A-The aortic arches connect the ventrally placed heart to the paired dorsal aortae. The
paired dorsal aortae fuse to form a single aorta caudally.
1st arch (Mandibular arch)- Maxillary artery
2nd arch (hyoid arch)- Hyoid & Stapedial artery.
3rd arch– Rt. & Lt. common carotid
4th arch- on the left side- Arch of aorta between the left CCA & Left
SCA
On the right side- Right SCA
5th arch – Both sides disappear.
6th arch– Pulmonary arteries & ductus
Q-Describe the surface marking of lungs.
A-Oblique fissure: anteriorly- 4th rib to anterior axillary line, posteriorly- the 6th rib (level
of posterior axillary line) to the vertebral border of the scapula
Upper lobe: above 4th rib
Middle lobe: between 4th & 6th rib
Lower lobe: below 6th rib

Q-What is the auscultatory triangle?
A-Is formed by:
- Lower margin of trapezius
- Vertebra
- Upper border of latissimus dorsi
Q-What is the meaning of term ‘Diaphragm’?
A-In greek; ‘Dia’ means thru’ & ‘phragma’ means partition.
Q-What is the meaning of term ‘Coarctation’?
A-In Latin coarctere means to contract.
Q-What is the importance of angle of Louis?
A-It corresponds to:
- The level of 4th vertebra
- Tracheal bifurcation
- Arch of aorta traverses the thorax from right to left in a posterolateral direction
- Site of 2nd ICS
Q-What is the nerve supply of the diaphragm?
A-The diaphragm is supplied by the phrenic nerves.
[Note:If quadriplegia also involves the diaphragm, it is termed as Pentaplegia.]
Q-When does the heart starts beating in an embryo?
A-22 days.
Q-Why is LA O2% 99% and not 100%?
A-Due to drainage into the PV & LA of the:
- Bronchial veins
- Thebesian veins

PHYSIOLOGY
Q-What is Ohms law?
A-Current= (potential difference)/ (resistance)
Q-What is Poiseulle’s law?
A-Flow is directly proportional to the 4th power of radius & inversely proportional to the
length of narrowing.
Hence,
Pressure= flow x impedance
Systemic BP= systemic flow (CoP) x SVR
SVR in Wood units
1 wood= 80 dynes.sec.cm-5
Q-What are the phases of a cardiac electrical cycle?
A-
Phase 0: rapid depolarization- due to influx of Na+
Phase I: initial repolarization- influx of Cl-
Phase II: plateau- balance of K+ outflow with Ca2+ inflow
Phase III: late repolarization- continuing K+ efflux
Phase IV: resting phase
Q-Describe ECG correlation with phase of electrical cycle.
A-is
Phase 0 & I- QRS complex
Phase II- ST segment
Phase III- T wave
Q-What is the rate of normal coronary blood flow?
A-It is 70- 90 ml/100 gm of myocardium/ min
Q-What is the rate of myocardial oxygen extraction?
A-
Normal myocardium- 75% extracted
Stressed myocardium- 100% extracted
Normally other organs- 25% extracted
[Note: Significance of above:Unlike other organs the myocardium cannot extract more
oxygen when required. It requires an increase in blood flow.]
Q-How is Ejection fraction calculated?
A-Ratio of stroke volume to end diastolic volume
[(EDV-ESV)/EDV] x 100
Normally 67  8%.
Q-Is normal endothelium negatively charged
A-Yes.

Q-What is the O2 demand of myocardium?
A-The O2 demand of myocardium is:
< 25ml/100gm/min- exercising
9 ml/100 gm/min- normal
3ml/ 100 gm/ min- beating empty (on bypass)
0.3 ml/ 100 gm/min- arrested with cardioplegia
Q-What is Ventricular remodeling
A-A series of physiologic adaptations of the ventricles to changes in ventricular filling
conditions.
Q-Why does the cardiac muscle not get fatigued?
A-Due to:
1) Increased blood supply
2) Increased number of mitochondria
Q-What is the contribution of the atrial contraction to CoP?
A-
Normally: 20%
In atrial fibrillation: 0%
In HOCM: 60- 70%
(Thus if a patient of HOCM develops atrial fibrillation, rapid development of pulmonary
edema)
Q-What is the normal pulmonary blood flow in a fetus
A-
- 1st trimester 0%
- 2nd trimester 3%
- 3rd trimester 10%
After birth PVR is 2/3rd of SVR.
Later it falls due to:
- Closure of PDA (within 2 weeks)
- Closure of PFO
Q-What is the saturation of veins at various sites in the body?
A-
- Coronary sinus= 25%
- Infrarenal IVC=60%
- Renal vein= 80%
- Suprahepatic IVC= 70%
Q-What is the normal PVR/ SVR?
A-= 2/10

Q-What is the definition of low CoP?
A-Post operatively, for convalescence, CoP required is:
- On POD1= 2 lit/min/m2
- On POD2= 2.5 lit/ min/m2
If CoP < 1.5 lit/min/m2 then the incidence of death is high
A mixed venous PO2 < 30 mm Hg is s/o low CoP & a mixed venous PO2 < 23 mm Hg
indicates a severe reduction of CoP.
Q-What is the relation of fever & metabolism?
A-For every 1C increase in temperature:
a) Metabolic rate increases by 12%
b) HR increases by 15 beats/ min
c) Insensible waterloss 300- 500 ml/m2/day

PROFORMA FOR HISTORY TAKING IN A LONG
CARDIAC CASE
THE BASIC OUTLINE
1) Personal particulars:
Name, age, sex, occupation, religion & residence.
2) Chief complaints:
Dyspnea,
Palpitations,
Cough with/ without expectoration,
Hemoptysis,
Chest pain,
Syncopal attacks.
3) ODP of each
4) H/o CCF
5) H/o Thromboembolic episode
6) H/o Infective endocarditis,
7) H/o cyanosis/ cyanotic spells/ squatting episodes
8) H/o Rheumatic fever
9) H/o Pressure symptoms- hoarseness of voice, dysphagia
10) Treatment history
11) Personal history
12) Family history.

NAME
For:
1) For establishing a rapport with the patient
2) May give an idea about the religion/ race
AGE
For:
1) Will give an idea about the illness & also helps in ruling out certain illnesses. Eg:
a. Syphilitic AR- Incubation period is ≈ 9 years. Thus considering an
infection at 11-12 years of age, the patient has to be a minimum of 20
years of age for a diagnosis of syphilitic heart disease.
b. RHD with valvular lesions is extremely rare before 5 years of age (Infact
the earliest RHD-MS requiring surgery was reported by Stanley John as 6
years in are view of 3724 pts undergoing CMC-in Circulation 1983 and
also the earliest RHD-MR requiring surgery was reported at 4 years by
Alain Carpentier in a review of 951 patients for reconstruction-in
Circulation 2001.)
c. A bicuspid AV degeneration is seen after the 3rd decade of life.
2) A decision about the prosthesis to be implanted depending upon the age.
3) In congenital heart disease, to get an idea about:
- Cyanosis, in a child, presenting at birth
- CCF present in a child (Eg. A newborn or infant with CCF will
suggest a large shunt)
SEX
For:
1) Certain ailments are more common in certain sexes. Eg:
a. Males have a higher incidence of:
- Hypetrophic subaortic stenosis
- Congenital valvar AS
- d TGA
- Coarctation aorta
b. Females have a higher incidence of:
- Osteum secundum ASD
- PDA
- Isolated MS
- Isolated MR
2) If the patient is a female of childbearing age, the advice of surgery (of any kind)
& also the type of surgery (type of valve) will vary.

OCCUPATION
For:
1) Respiratory ailments.
2) Sedentary lifestyle- higher chances of coronary artery disease.
RELIGION
For:
If a bioprosthetic valve is being planned then
- In a Muslim- a porcine valve may not be preffered, &
- In a Hindu- a bovine valve may not be preffered.
RESIDENCE
For:
1) Higher attitude patients have a higher tendency for Secundum ASD’s & also
earlier development of PH in the same.
2) Higher attitude patients have a higher tendency for PDA
3) People from tropical areas (Eg: Kerala) have a higher incidence of
endomyocardial fibrosis.
4) Aortoarteritis is more common in south India
5) Hydatid cyst is commoner in Punjab & Madurai.
DYSPNEA
Definition: Abnormally uncomfortable awareness of ones own breathing.
Divided into 4 grades, similar to NYHA classification.
NYHA classification: The New York Heart Association: has 4 components, viz;
Dyspnea, palpitations, fatigue & angina.
Presently followed is the 7th edition of NYHA (laid down in 1994.)
NYHA I: In a patient with heart disease with no limitation of physical activity. Ordinary
physical activity does not cause dyspnea, palpitations, fatigue or angina.
NYHA II: In a patient with heart disease with mild limitation of physical activity.
Comfortable at rest but ordinary physical activity causes dyspnea, palpitations, fatigue or
angina.
NYHA III: In a patient with heart disease with moderate limitation of physical activity.
Comfortable at rest but less than ordinary physical activity causes dyspnea, palpitations,
fatigue or angina.
NYHA IV: In a patient with heart disease with marked limitation of physical activity.
Symptoms are present at rest & increase on exertion.
[Note:PND is not included in the NYHA classification.]

Q-Is there any classification besides NYHA?
A-The following are the classification systems:
1- Canadian cardiovascular society classification CSS - only angina (of)
2- Specific activity scale (of Goldman)- most specific- calculation of metabolic
equivalents (1 MET= 2.5 ml/ Kg/ min)
Dyspnea is cardinal manifestation of LV failure. The increase in severity is in the
following order:
Dyspnea on exertion → PND → Orthopnoea → Dyspnea at rest → pulmonary edema.
Orthopnoea:
In the recumbent position there is decreased pooling in the lower limbs & abdomen →
blood is displaced from extrathoracic compartment to thoracic compartment →
Failure of LV to pump blood →
Increased pulmonary venous congestion & capillary pressure →
Interstitial edema → leading too:
1) Decrease in lung compliance +
2) Increase in airway pressure +
3) Ventilation perfusion mismatch.
→ all leading to dyspnea.
It occurs rapidly, within1-2 minutes of lying down & is relieved on sitting.
Cough accompanies due to increased pulmonary congestion.
A non-productive cough present in CCF is considered as “ dyspnea equivalent” and in
recumbency is considered as “ Orthopnea equivalent”
Trepopnea:
Orthopnea limited to one lateral position. ? due to distortion of great vessels.
Platypnea:
Dyspnea relieved on lying down. Reasons are not known.
Paroxysmal nocturnal dyspnea:
The patient awakes suddenly with a feeling of severe anxiety & breathlessness.
Associated bronchospasm (due to edema of bronchial mucosa) may be present.
[Note:Also called as cardiac asthma due to associated wheeze.]
It receives a longer time to get relieved. Reasons for PND are:
1) Slow absorption of extracellular fluid from the dependent areas & resultant
increase in blood volume
2) Elevation of diaphragm
3) Decrease LV adrenergic support during sleep
4) Depression of respiratory center during sleep
5) Transient nocturnal arrhythmias.

Q-What are the reasons for dyspnea in CCF/ LVF?
A-
1) Pulmonary function depressed → increased interstitial fluid → decreased lung
compliance → increase airway pressure.
2) Respiratory muscle dysfunction.
COUGH
For:
1) Feature of LVF- considered as dyspnea equivalent.
2) Impending pulmonary edema
3) Chronic bronchitis
4) Brassy cough relieved on bending forward- arch aneurysm
1), 2) & 4) are posture related.
HEMOPTYSIS
Definition: Expectoration of blood.
Ranges from streaky blood stained sputum to gross hemoptysis.
Types: True- tracheobronchial & alveolar
False- oral/ nasopharyngeal
Q-What are the causes of hemoptysis in a patient with MS?
A-Causes of hemoptysis in a patient with MS/ LVF (Paul Wood, 1954) are:
1) Pulmonary apoplexy/ sudden hemorrhage- profuse, rarely life threatening, due to
rupture of dilated thin walled bronchial veins caused by acute rise in left atrial
pressure. (This is not seen generally due to chronicity which causes the vein walls
to become thick)- stops on its own.
2) Blood stained sputum associated with PND.
3) Pink frothy sputum seen in pulmonary edema due to rupture of alveolar
capillaries.
4) Pulmonary infarction- due to PA embolism.
5) Following chronic bronchitis due to edematous bronchial mucosa.
CHEST PAIN
Chest pain may divided into 3 categories-
- Ischemic cardiac
- Non ischemic cardiac
- Non cardiac

Ischemic cardiac:
1) Coronary artery disease (decrease supply)
2) LVH/ RVH (increase demand)
Non ischemic cardiac:
1) Pericarditis
2) Dilatation of the PA
3) Dissection of aorta
Non cardiac:
1) Pulmonary embolism
2) Pleural
3) Esophageal
4) Skeletal
PALPITATIONS
Definition: Awareness of beating of ones own heart.
Occurs due to following cardiac physiological alterations:
1) Change in heart rate
2) Change in rhythm &
3) Augmentation of contractility
Other causes of palpitations are:
-Thyrotoxicosis
-Hypoglycemia
-Fever
-Drugs
Q-What are causes of palpitations in the first decade of life?
A-Possible causes are:
1) RHD with vale affection
2) Ebsteins
3) C-TGA
SYNCOPE
Definition: An association of:
- Generalized weakness of muscles with a loss of postural tone
- Inability to stand upright &
- A loss of consciousness.
Q-What are the causes of syncope in a cardiac patient?
A-Cardiac causes of syncope maybe due to:

1) Decreased cardiac output:
- LVOT obstruction- AS, hypertrophic subaortic stenosis
- Obstruction to pulmonary blood flow- severe PS/ pulmonary
atresia, cyanotic spell, pulmonary embolism
- Myocardial- massive MI
- Pericardial- tamponade
2) Arrhythmias:
- Bradyarrhythmias
- Tachyarrhythmias
3) CNS- embolism/ hypoperfusion
- LA thrombus, arch aorta aneurysm with thrombus
- LA myxomas
- Vegetations
- Others- carotid artery stenosis, vasovagal, rupture of IC
aneurysm due to hypertension.
H/O CONGESTIVE CARDIAC FAILURE
Ask history in form of:
- Edema feet & puffiness of face
- Distension of abdomen
- Pain in the right upper abdomen
- Anorexia, nausea & vomiting
- Chest pain (15% of cases of CCF) due to RVH
- Oliguria & nocturia (due to fluid retention with redistribution at night)
Q-Who proposed the forward & backward failure theory of CCF?
A-
Backward theory- James Hope (1832)
Forward theory- Mackenzie (1913)
H/O THROMBOEMBOLIC EPISODES
Ask for affection of the following organs:
1) CNS- loss of consciousness
- Transient (TIA)
- Prolonged with neurological deficit
- Convulsions
2) Other organs:
- Hematuria
- Abdominal pain
- Limb pain
- Coronary pain

Q-What are the ‘intracardiac’ causes of systemic embolization?
A-Intracardiac source of embolus may be in from of:
1) Thrombus
2) Vegetations
3) Myxomas
4) Paradoxical embolism
5) Plaques (rarely)
Q-Are a particular subset of patient more prone embolization?
A-Yes.
Tendency for embolization is directly related to:
- Age
- Size of LAA
- Atrial fibrillation
Tendency for embolization is inversely related to:
- Cardiac output.
Q-Discuss the characteristics of thromboembolism secondary to intracardiac clots.
A-It is usually the fresh clot that embolize (only a minority of patients with h/o recent
TEE have clots found in the LAA).
50% of TEE are cerebral & is recurrent/ multiple in 25% of above.
Q-Which is the commonest cyanotic congenital heart diseases to produce CNS
complications?
A-
1) Tricuspid atresia- 35% incidence beyond the age of 3- 4 years)
2) TOF
H/O INFECTIVE ENDOCARDITIS
Definition: A microbial infection of the endocardium.
1st stage in the formation of non thrombotic bacterial endocarditis (NBTE), which gets
infected later.
NBTE form over areas of:
- Endocardial injury
- Turbulence
Areas of affection:
- Tends to occur in high-pressure areas; thus more on the left side.
- Areas where the blood flows thru’ a narrow orifice; from high to low pressure. Eg.
distal to a coarctation, in VSD on the RV side, for PDA on the PA side.
Q-In which condition is endocarditis rare?
A-Endocarditis is rare in low flow states, eg., ASD.

Q-Discuss clinical features of IE.
A-The clinical features of IE are due to:
1) Constitutional features of infection,
2) Local destruction
3) Embolization of vegetation leading to
- Infarction
- Infection
4) Other area of infection due to persistent bacteremia
5) Immune reactions.
Thus the symptoms of IE are:
- Onset after ≈ 2 weeks of precipitating event
- gradual onset with mild fever & malaise if the organism is of low virulence
(streptococcus) or acute onset with high fever if the organism is of high pathogenecity (
staph)
- Fever- low or high, is present in all patients with IE. (*except in elderly, congenital
heart disease, fungal IE)
- Fever is generally low grade (< 39.4°C)
- Arthralgia & arthritis
- Symptoms of embolization are:
- Hematuria
- Hematemesis
- Limb ischemia.
- Worsening of symptoms/ CCF- due to leaflet destruction
Q-What are the signs of IE?
A-The signs of IE are:
- Constitutional- fever
- Local destruction resulting in –
- new murmur
- change in preexisting murmur
- CCF
-Splenomegaly & petechia ≈ 30% of patients with long duration. Petechia are usually
seen on conjunctiva, palate, buccal mucosa, upper extremity.
-Roth spots- over retinal hemorrhages with clear center.
-Osler nodes- tender nodules on fingers/ toe pads- believed to be due to deposition of
immune complexes
-Janeway lesions- seen in acute endocarditis- are small hemorrhages with nodular
charater seen on palm & soles.
-Clubbing- long standing disease.
-Embolization- especially pulmonary emboli are seen in IV drug abusers with Rt. sided
IE & in also from Lt. sided IE with a Lt.→ Rt. shunt.
-Mycotic aneurysm
-CNS manifestation- due to embolization & cerebral abscess
-Glomerulonephritis- due to immune complexes & embolization

Q-What are characteristics of endocarditis?
A-Endocarditis occurs more frequently in regurgitant lesions than stenotic lesions & is
characteristically on the atrial surface of MV & ventricular surface of AV.
Q-What is D/D of IE?
A-
- Acute rheumatic fever
- Myxomas
Q-What are the procedures, that do not require antibiotic prophylaxis, in a patient with
prosthetic valves?
A-They are:
- Dental picking
- Upper GI scopy
- Primary bronchoscopy
- Clean surgery- Eg. Elective cesarean section
- Shedding of primary tooth
- IUCD insertion
Q-Discuss antibiotic prophylaxis for various invasive procedures.
A-
For oral/ dental/ upper GI procedures:
Regimen I: 3 gm Amoxycillin prior & 1.5 gm Amoxycillin 6 hours post procedure
Regimen II: 1 gm Erythromicin prior & 500 mg E’mycin 6 hours post procedure
For lower GI/ GUT procedures:
Regimen I: IV Amoxycillin (3 gm) + IV Genta (1.5 mg/Kg) ½ hour prior to the procedure
& 1.5 gm Amoxycillin 6 hours post procedure.
Regimen II: IV Vancomycin (1 gm) + IV Genta (1.5 mg/Kg) ½ hour prior to the
procedure.
Q-No IE prophylaxis is required in which cardiac lesions?
A-
1) ASD- unoperated or operated
2) MV prolapse
3) Coronary artery disease/ post CABG
Q-Classify postoperative IE?
A-IE can be classified as:
Early < 60 days postoperative
Late > 60 days postoperative
Early is due to intraoperative or immediate postoperative contamination.
Mechanical > Bioprosthetic > Homograft IE is more in the early period
However in the late period, IE is equal in all the kinds of valves.

Q-Discuss the treatment of IE.
A-
Streptococcal: Penicillin G 6 lac units 6 hourly- 4 weeks +/- Gentaminicn 1.5 mg/
Kg/day
Staphylococcal: Vancomycin 15 mg/Kg/dose 12 hrly- 4 weeks +/- Gentaminicn 1.5 mg/
Kg/day
Q-What are reason for postponing cardiac surgery in patient’s with IE who otherwise
require surgery for endocarditis?
A-
1) CNS- acute hemorrhagic stroke (< 10 days)
2) Renal- Acute glomerulonephritis leading to renal failure.
3) Thrombocytopenia
H/O CYANOSIS & CYANOTIC SPELLS
Definition: Bluish discoloration of nails, skins & mucus membranes due to an increase in
the amount of reduced hemoglobin (< 5 gm%) in the capillary blood.
Types:
- central - peripheral
- abnormal pigments -mixed
-differential
Pathophysiology: When the amount of reduced Hb is > 5 gm% the blood appears dark,
giving the tissues a bluish hue. This is seen earliest in the warm areas (areas with
increased capillary circulation.)
Q-What is the etiology of peripheral cyanosis?
A-Peripheral cyanosis is due to slowing of blood; hence causing increased tissue O2
extraction. This is visible over the nose tip, ear lobule & tips of fingers.
Q-What are the causes of central cyanosis?
A-Causes of central cyanosis are:
1) Cardiac-
a. Congenital cyanotic
b. Eisenmengerization
c. CCF
2) Pulmonary-
a. COPD
b. Bronchiectasis
c. Massive collapse & fibrosis
3) High altitude

Q-What are the causes of peripheral cyanosis?
A-Causes of peripheral cyanosis are:
1) Cold/ vasoconstriction
2) Shock
3) Increased viscosity of blood
Q-What are the causes for mixed cyanosis?
A-Causes are-
1) Acute LVF
2) Severe MS (incipient pulmonary edema & vasoconstriction)
Q-What are the abnormal pigments that can produce cyanosis like picture?
A-They are:
Methhemoglobin, sulphhemoglobin etc.
Q-Discuss ‘differential cyanosis’?
A-It is seen in-
1) Only of lower limbs with/ without left upper limb in
- PDA with PH with Rt. To Lt. Shunt. With preductal coarctation
- Severe coarctation
2) Only upper limbs in
- PDA with PH with rt. to lt. Shunt along with TGA
- Coarctation with TGA
Q-What is the D/D between central cyanosis & peripheral cyanosis?
A-In central cyanosis there is:
1) Good peripheral warmth
2) Clubbing
Q-Which are the conditions were cyanosis cannot occur?
A-Cyanosis cannot occur in:
1) Severe anemia (Hb< 5 gm%),
2) Carbon monoxide poisoning
[Note:In Indians cyanosis is apparent when the O% is < 85%. When < 65%, intense
cyanosis.]
Q-In which conditions a patient may appear blue but there is no cyanosis?
A-The conditions are:
1) Sulphhemoglobinemia/ methhemoglobinemia
2) Silver poisoning
3) Aniline dye workers
4) Extreme cold environment

Q-Which conditions can mask cyanosis?
A-
1) Anemia
2) Dark complexion.
CYANOTIC SPELLS
Synonym: Hypoxic spell/ paroxysmal hyperapnea
Q-Define cyanotic spell?
A-A typical spell is characterized by a progressive increase in rate & depth of respiration
& culminates in paroxysmal hyperapnea, deepening of cyanosis, limpness, syncope &
occasionally convulsions or death.
Q-What does the EEG during a spell reveal?
A-EEG during a spell is similar to that of an acute hypoxic episode.
Q-Does the incidence of cyanotic spell vary with age?
A-The incidence of cyanotic spells increases after 2-6 months of age due to:
1) Replacement of fetal Hb by adult Hb
2) More activity of child
3) Closure of PDA
& decreases after 2 years of age due to:
1) The os infundibulum getting fixed (fibrotic changes in the infundibulum)
2) Child has learned as to how to avoid a spell
3) Collaterals grow
4) Improved Hb
Q-Which conditions are associated with cyanotic spell?
A-Cyanotic spells are seen in:
-Tetrology of Fallot - DORV, VSD, PS - VSD, PS
- TGA, VSD, PS - ASD, PS - TA Ib/IIb
Q-What are the triggering factors for cyanotic spells?
A-The triggering factors for a cyanotic spell are:
1) Spontaneous
2) Crying
3) Feeding
4) Bowel movements
*particularly seen if stress occurs immediately after an infant has waken up from a long
deep sleep.

Q-What are the various theories of cyanotic spell?
A-The theories of spell are:
1) Proposed by Guntheroth & Morgan: presence of a vulnerable respiratory control
mechanism, which is especially sensitive after a prolonged sleep.
It reacts to a sudden increase in cardiac output (occurring due to waking up from sleep)

Increased venous return

Increased Rt. To Lt. Shunt

Fall in PO2 and rise in PCO2

Hyperapnea

Increased CoP
A vicious cycle sets in with the increased CoP leading to increased venous return.
2) Proposed by Wood: There is infundibular spasm due to increased sympathetic
activity (this theory does not explain the spells in pulmonary atresia)
3) Proposed by Young: Atrial tachycardia leading to increased right to left shunt.
4) Decreased RV diastolic filling due to dehydration.
Q-Describe the treatment of spell.
A-The treatment consists of:
O2
+
Knee chest position
+
Morphine/ buprenorphine (0.1 mg/ Kg, max up to 0.2 mg/ Kg, not to be repeated within 4
hrs)
+
NaHCO3- 1-2 meq/Kg/ dose

IV Propranolol 0.05- 0.1 mg/ Kg/ dose, slow IV +/ -
IV Phenylephrine 1-3 ug/ Kg infusion

Ketamine –2 to 10 mg/ Kg & Intubation

BT shunt
Other options available are:
- If duct dependent- PGE1/ duct stenting
- If TGA- BAS
Q-Is the mortality of emergency BTS higher than that for elective shunt?
A-Yes, the mortality for an emergency BT shunt is much higher than for an elective shunt
(15% vs. 1%)

Q-Describe the prevention of cyanotic spells.
A-The following will help in preventing repeated spells:
1) Avoid precipitating cause- eg. Vasodilators
2) Iron supplements
3) Treat RTI promptly
4) Blood letting
5) Optimization of propranolol therapy
6) Plan surgical management
Q-Which drugs worsen cyanosis?
A-The following worsen cyanosis:
1) Digoxin
2) Vasodilators
SQUATTING EPISODES
Q-Discuss ‘squatting episodes’?
A-History of squatting, for relief of symptoms, is hallmark of Tetrology of Fallot.
Squatting helps by:
1) Increasing the SVR by kinking the femoral arteries decreasing the rt. to lt. Shunt.
2) Decreased return of a more deoxygenated blood to the heart from the lower limbs,
by kinking the femoral veins.
3) Pushing relatively ‘more oxygenated’ venous blood from the abdominal viscera to
the heart,
4) Relaxation of sympathetic overdrive by resting.
Q-What are the various ‘squatting equivalents’?
A-They are the following:
3 were described by Taussig in 1947:
1) Knee chest position while sitting on the ground
2) Legs folded underneath the body (like a ‘namaz’ position)
3) Lying down.
2 more added, to the list, by Lurie in 1953:
4) Standing with legs crossed
5) Parent holding the baby against owns abdomen with the babies LL flexed.
Q-What are the types of squatters?
A-There are 2 types of squatters:
Rapid- mainly adult, &
Slow

H/O RHEUMATIC FEVER
-Ask for h/o sore throat followed by fleeting arthritis.
Definition: It is an acute non-suppurative immune mediated inflammatory disease,
usually in children, that follows a few weeks after an attack of pharyngitis; caused by
group A  hemolytic streptococci.
Q-What are the reasons for increased prevalence in developing nations?
A-The exact reasons are not known. It is believed to be due to:
- Increased urbanization (due to increased droplet infection),
- Overcrowding ( ” ).
[Note:There is no proof to suggest that nutritional factor has a role in RF.]
Q-Discuss the etiopathogenesis of RF.
A-The causative agent is group A  hemolytic streptococci however in 1/3rd of the
patients there is no h/o sore throat nor blood culture yield e/o streptococcal infection.
Pathogenesis is not known & is believed to be an immune reaction to bacterial allergy or
an autoimmunity.
Q-Describe Aschoff bodies.
A-Aschoff bodies have the following features:
- May be seen if there is cardiac involvement secondary to RF
- Seen in the myocardium & endocardium (rarely over the valves)
- Most frequently seen in the; IVS & posterior surface of LV/ LA.
- They are discrete lesions, < 1mm diameter, formed by a collection of round cells,
fibroblasts & MN giant cells, surrounded by a zone of PMN cells & lymphocytes.
- Particularly situated around small blood vessels.
Q-What are the clinical features of RF?
A-The clinical features of rheumatic fever are:
- symptoms begin usually 2-3 weeks after an episode of acute pharyngitis.

-fever (is always present, except in chorea)

-fever lasts for 2-3 weeks.
-Other features that may follow are:
1) Arthritis: It is a fleeting arthritis affecting large joints with no residual deficit.
Generally affected joints are:
- Knee
- Ankle
- Elbow
- Wrist
Each joint remains inflamed for 1-7 days & complete episode lasts for  3 weeks.

Q-RF can affect which other joint?
A-RF can rarely affect the following joints:
- Shoulder
- Hip
- Small joints.
*Rarely a deformity may be left behind- Jaccoud’s arthritis.
2) Subcutaneous nodules: (These are considered pathognomic of rheumatic fever.)
They are:
- Less than 2 cm diameter
- Freely mobile overlying skin
- Site: Over bony prominences especially skull, galae aponeurotica.
For examining for these nodules, ask the patient to squat & keep the elbows on the knees
& wrists folded beneath the chin. Now palpate the shin, extensor aspect of elbow, occiput
& mid back, i.e., over & around the spine & scapula.
3) Erythema marginatum: These are:
- rapidly evolving small macules papules  large circles with raised & well
defined edges which blanch on pressure.
- Disappear within few hours.
- Site; trunk, limbs. Very rare on the face.
4) Chorea (St. Vitus dance): These are:
- Characterized by involuntary, non repetitive, jerky movements which decrease
during sleep and increase with anxiety.
- In children any gender, but post puberty mainly in girls,
- The patient becomes irritable & produces jerky movements, grimacing
involuntarily & has slurred speech.
- Generally seen along with carditis or nodules.
Q-How can rheumatic chorea be diagnosed clinically?
A-When the child is asked to extend the arms there is a tendency to flexion at the wrist &
hyperextension of the fingers.
Q-Who was St. Vitus?
A-St. Vitus was a roman catholic priest who patronized epileptics & actors.
5) Carditis:
It is essentially a pancarditis.
50% of cases of rheumatic fever have carditis.
Endocarditis-
¾ th of patients developing carditis have a new murmur, which may be
- Apical pan systolic murmur; due to myocarditis (the commonest murmur)
- Apical mid diastolic murmur, Carrey Coombs murmur,
- PA systolic murmur, due to fever, anemia.

Myocarditis-
- Important feature of myocarditis is progressive dilatation of LA & LV.
Pericarditis- 2 types
- Acute fibrinous
- Effusion
(pericarditis is associated with severe forms of carditis.)
Q-What is the incidence of CCF in patients with rheumatic carditis?
A-CCF occurs in 10% of patients with rheumatic carditis.
[Note:Prolongation of PR interval is temporary but may persist for months (reason is not
known)]
[Note:Rheumatic fever may lick the joints but certainly bites the heart.]
[Note:Rheumatic fever mainly affects the left side of the heart (reason unknown)]
Q-Discuss Jones criteria.
A-
Original criteria were described by T. Duckett Jones in 1944.
Currently the 4th edition (updated in 1992) of Jones criteria is accepted.
The criteria is as follows:
Major Minor
Carditis Clinical-
- Fever
- Arthralgia
- H/o rheumatic fever/RHD
Polyarthritis Investigations-
- Presence of acute phase
reactants (CRP, ESR, leucocytosis)
- PR interval prolongation
Subcutaneous nodules
Erythema marginatum
Chorea
+
E/o of streptococcal infection, in form of
- ASLO +ve, or
- + ve throat culture, or
- h/o scarlet fever.
The diagnosis of rheumatic fever, by modified Jones criteria, is by
- 2 major criteria + e/o streptococcal infection, or
- 1 major & 2 minor criteria + e/o streptococcal infection.
If there is no supporting e/o streptococcal infection then a diagnosis of rheumatic fever
should not be accepted, except in 2 conditions:
- only signs of chorea, or
- only signs of carditis.

(This is because the infection may have occurred few months back & hence the antibody
titres may have returned too normal.)
[Note:In India polyarthralgia is included as major criteria (in 1994 by Padmavati &
Khanna)]
Q-What is average duration of rheumatic fever?
A-The average duration of an attack of rheumatic fever is 3 months. In cases of carditis, it
may continue for nearly 6 months.
Q-Discuss ASLO.
A-Described by Todd in 1932.
Normal levels are upto 333 Todd units- in children &
Upto 250 Todd units in adults.
Most specific test for rheumatic fever is AntiDNAase antibody levels.
Normal levels are upto 240 Todd units- in children &
Upto 120 Todd units in adults.
Q-What is the D/D of streptococcal pharyngitis?
A-
- viral: characterized by more malaise & rhinitis.
- Other bacterial.
Q-What is the risk of recurrence of RF?
A-Risk of recurrence of rheumatic fever is 65% & subsequently the risk decreases with
time.
Q-What are the WHO recommendations for rheumatic fever?
A-The WHO recommendations are to treat all sore throat as due to group A  hemolytic
streptococci unless proved otherwise. The prophylaxis is:
Single injection of 12 lac units Benzathine penicillin (if wt. > 27 Kg) &
Single injection of 6 lac units Benzathine penicillin (if wt. < 27 Kg)
Or
Oral Erythromycin 20 mg/Kg/day for 10 days.
Q-Discuss the treatment of rheumatic fever.
A-Treatment of rheumatic carditis is 3 fold:
1) Treatment of CCF- bed rest, salt restriction, digoxin, diuretics
2) Treatment of Carditis- Aspirin- 100 mg/kg/day in 8-10 divided doses for 1 month
 if symptoms persist after few days of starting aspirin  add Prednisolone 1-2 mg/ Kg/
day & reduce aspirin.
3) Treatment of rheumatic fever.
Q-What is the incidence of valvular affection of RHD?
A-The incidence of valvular affection of RHD:
MV- 70-80%, MV + AV- 20- 25%,
Only AV- 5- 8%, TV- 30- 50% (autopsy)

Q-Which places in India have a high prevalence of RHD?
A-The areas are:
- Kutch
- Dhulia
Q-What are the first auscultatory manifestation of carditis in rheumatic fever?
A-They are:
1) Pansystolic murmur of MR (between Grade 2-4)
Occasionally
2) Carrey Coombs murmur &
3) Flow murmur across the PV
PRESSURE SYMPTOMS
These are
- Hoarseness of voice &
- Dysphagia
Q-What is hoarseness of voice, secondary to cardiac cause, termed as?
A-Otner’s syndrome.
Q-What are the causes of hoarseness of voice in a cardiac case?
A-Reason for hoarseness are:
Due to compression on the left recurrent laryngeal nerve by
- Dilated LA
- Tracheobronchial LN
- Enlarged PA
- Arch aorta or proximal descending thoracic aortic aneurysm
- Aneurysm of ductal ampulla
Q-Enumerate the cardiac related reasons for dysphagia?
A-Due to pressure on esophagus by:
- Arch/ descending thoracic aortic aneurysm
- Aberrant Rt. Subclavian artery- dysphagia lusoria
- LA enlargement
- Rt. Aortic arch
TREATMENT HISTORY
Ask for
- Drugs taken
- Since when
- Any surgical procedure advised or performed.

MEDICAL ILLNESS IN PAST
Ask for
- Diabetes- important for CAD, post operative wound healing
- Hypertension
- Tuberculosis- ask for presence of low grade fever with/ without rigors in evening,
anorexia, weight loss, hemoptysis, scars or sinuses.
- Syphilis
- Bleeding disorder- for intra op & post op anticoagulation
- Hematemesis/ malena- for intra op & post op anticoagulation
- Maternal diabetes- higher incidence of child having TGA, VSD
- Maternal SLE- higher incidence of child having congenital complete heart block
- Drugs taken & illness during pregnancy (see below).
Q-What is the importance of maternal illness & treatment history during gestation?
A-
Significant illness during pregnancy: Rubella can cause congenital rubella syndrome
Importance of drugs during pregnancy:
Drug Fetal cardiac anomaly Associated defects
Alcohol VSD Growth & mental
retardation,
microcephaly
Phenytoin PS, AS, coarctation, PDA Hypertelorism, growth &
mental retardation
Lithium Ebsteins, Tricuspid atresia
Thalidomide# Tetrology of Fallot/
Truncus
Phacomelia
Warfarin PS, PDA Teratogenic
#Thalidomide has been reintroduced for the treatment of – erhythema nodosum leprosum,
multiple myeloma.
Q-What are the teratogenic effects of warfarin?
A-They are:
1st trimester- affects cartilage development, additional CVS malformations (PDA, PS)
2nd trimester- still born, spontaneous abortion, CNS abnormality (? Due to IC bleed).
PERSONAL HISTORY
Ask for history of paan consumption as;
- paan contains betel nut which is rich in aracholine, which in turn may lead to
bronchospasm.

FAMILY HISTORY
Significance of family history is for
- Coronary artery disease
- Congenital heart disease,
- Consanguineous marriage,
- Age of the parent; at time of birth of child (patient).
Q-Discuss the importance of family history for congenital heart disease?
A-(From an article by Nora & Nora, Circulation 1978)
The % risk of an offspring having a CHD if the parent has the disease:
Disease % in offspring if father is % in offspring if mother is
affected affected
Congenital AS 3% 13%
ASD 1.5% 4.5%
AV canal 1% 14%
Tetrology of Fallot 1.5% 2.5%
VSD 2% 10%
PDA 2.5% 4%
The % of risk of a baby being affected if a sibling is affected:
Disease % in 1st sibling % in 2nd sibling
ASD 3% 8%
Tetrology of Fallot 3% 8%
VSD 3% 10%
PDA 3% 10%
[Note:If a parent & sibling, both are involved then the risk of another sibling having the
heart disease is very high.]
Q-What is the importance of consanguineous marriage?
A-The importance lies for autosomal dominant & recessive conditions.
For autosomal dominant conditions like:
- Holt Oram syndrome
- Noonans syndrome
- Williams syndrome
- Marfans syndrome.
For autosomal recessive conditions like:
- Ellis Van Creveld syndrome,
- Kartegners syndrome
Q-What is the significance of age of parents?
A-The significance of age is as follows:
- Increased paternal age: Higher incidence of Noonan’s
- Increased maternal age: Higher incidence of Down’s syndrome

PROFORMA OF GENERAL EXAMINATION
1) Built & nutrition
2) Temperature
3) Pulse- site, rate, rhythm, character, character, radio radial delay, radio femoral
delay, apex pulse deficit, condition of vessel wall, peripheral pulsations.
4) Respiration
5) Blood pressure- site & body decubitus,
6) JVP
7) Pallor
8) Icterus
9) Clubbing
10) Cyanosis
11) Signs of CCF
12) Peripheral signs of wide pulse pressure
13) Signs of Marfans
14) Signs of tuberculosis
15) Facial/ skeletal abnormality.

BUILT AND NUTRITION
Describe that-
- The patient is comfortably sitting in bed,
- The built of patient (optional)
Q-What are the postures, of significance, in a cardiovascular case?
A-
- Leg hanging down- in PVD,
- Squatting
Q-What are types of built?
A-Types of built are:
- Ectomorphic- light bones, small stature,
- Endomorphic- stocky, increased soft tissue,
- Mesomorphic- between the two.
Q-What are the parameters of ‘nutrition’
A-They are:
- age dependent- weight, height
- age independent- arm circumference
Q-How is the estimated weight & height of child for an age calculated?
A-The following formula may be followed for weight:
At birth= 2.5- 3.5 kg A-Age in years
3- 12 months- (A + 9)/ 2
1- 6 years- 2A + 8
7- 12 years- (7A- 5)/ 2
Height chart- estimated height of child for the age is as follows;
At birth- 50cm,
At 1 year= 75 cm
At 2 years= 85 cm
1-12 years= (Age x 6) + 77 cm
Q-How is the arm circumference measured?
A-Using Shakirs tapes for that age- there are 3 zones comprising of red, orange & green.
Q-Define ‘low birth weight’?
A-Weight < 2.5 Kg is considered low birth weight.
(In India, 30-35% of newborn are low birth weight)
Q-What is very low birth weight?
A-Weight of <1.5 kg is considered very low birth weight.

Q-Discuss normal ‘milestones’.
A-Normal developmental milestones are (in general & in brief):
1 mnth- when made of sit with support cannot hold head, but recognizes faces & smiles
4 mnths- can sit with support & hold head
8 mnths- can sit on own hands in front.
10 mnths- sit up on own with hands folded & can say monosyllables (mama/ dada)
12 mnths- stands & takes steps with support
18 mnths- walk on own
2 years- runs & talk toilet
3 years- climb stairs up- one stair with the same foot
4 years- climb stairs down- one stair with the same foot
5 years- can stand on 1 leg, dresses & undresses
6 years- stands on one leg with eyes closed. Counts till 20- 30.
Q-What are the congenital disorders which are associated with cardiac pathologies &
additional systemic manifestations (that might be evident on clinical examination)?
A-They are:
a) Muscoloskeletal
Disorder Cardiac defect Other abnormality
Holt Oram syndrome ASD Hypoplastic thumb
& radius
Ellis Van Creveld syn ASD Dwarfism &
polydactly
Noonans PV dysplasia Web neck, pectus
excavatum
Kartegners Dextrocardia Sinusitis,
bronchiectasis
b) Connective tissue
Marfans AR Mentioned later
Osteogenesis imperfecta AR Dwarfism &
polydactly
Ehler Danlos MR Hyperelastic skin
Pseudoxanthoma
elasticum
Arterial wall disease
c) Endocrine
Hypothyroidism CCF, bradycardia
Hyperthyroidism Atrial fibrillation
Cushings Hypertension
Addisons Hypotension
Phaeochromocytoma Hypertension

d) Metabolic & chromosomal
Mucopolysaccharoidosis Multivalvar Physical & mental
retardation
Downs Endocardial cushion
defects
Turners Coarctation
Q-Describe ‘characteristic’ facial abnormalities that maybe seen in a cardiac case?
A-
Facies Cardiac Disorder
- Elfine facies Williams syndrome
- Conotruncal facies AV cushion defects-TOF/ TGA/ DORV/ TA
- Downs syndrome Endocardial cushion defects
- Turners syn (slanting eyes Coarctation
micrognathia, web neck)
- Di Georges syndrome Truncus
(conotruncal facies)
- Noonans syn (hypertelorism PV dysplasia
low set ears, slanting eyes)
Q-What comprises conotruncal facies?
A-The following features makeup for conotruncal facies:
- low set ears,
- slanting eyes,
- periorbital edema,
- slit mouth
PULSE
Definition: A wave produced by cardiac systole that advances in the peripheral arterial
tree in the peripheral direction.
The components of a description of pulse include:
1) Rate: Normal 60 –90 beats/ min
*Tachycardia in a.f.- if ventricular rate> 85/ min
2) Rhythm:
- Regularly regular- nsr
- Irregularly irregular- a.f.
- Regularly irregular- Unifocal ectopics

3) Volume:
High volume in-
- AR, MR, PDA, VSD
- High output states- fever, anemia, pregnancy, Beri beri, thyrotoxicosis
- Increased stroke volume- complete heart block
Low volume in-
- LVOT obstruction
- Myocardial cause
- Pericardial
Varying volume in:
- Pulsus alterans- sinus rhythm of alternating beats of varying volume- seen in LVF
4) Character:
Normal pulse has
a- anacrotic wave
t- tidal wave
n- dicrotic notch
d- dicrotic wave
Q-What are various types of pulses?
A-
a) Anacrotic pulse- slow rising well sustained- seen in AS
b) Dicrotic pulse- 2 beats palpable; the percussion wave & the dicrotic wave- seen in
fever, CCF
c) Pulsus besferiens- 2 betas palpable in systole, rapidly rising pulse; the anacrotic
wave & the tidal wave- seen in AS with AR, idiopathic hypertrophic subaortic stenosis.
d) Pulsus parvus et tardus- slow rising & slow falling- seen in AS
e) Pulsus alterans- alternate strong & weak pulsations- seen in LVF
f) Pulsus bigeminus- regularly irregular with high volume- seen in unifocal ectopics.
g) Pulsus paradoxus- Normally the systolic BP falls by 10 mm Hg during inspiration.
This phenomenon is seen due to:
i. Increased venous return to the right heart & pooling in
the PV circulation decreased return to LA/LV 
decreased CoP.
ii. Movement of the IVS to the left due to RV filling 
decreased LV filling.
When the SBP falls more than 10 mm Hg, in inspiration, it is termed as pulsus paradoxus.
It is a misnomer, as it is nothing but exaggeration of the normal.
(*The paradox is that while the heart sound is heard, the pulse may not be felt)
Q-What are causes of pulsus paradoxus?
A-Causes are:
1) Cardiac- tamponade, constrictive pericarditis.
2) Pulmonary- Asthma, emphysema
3) SVC obstruction
[Note:Reverse pulsus paradoxus- It is seen in patients with CPAP, on ventilator]

h) Waterhammer pulse- rapid upstroke & rapid downstroke, characteristic rapidly
rising & rapidly falling pulse with high volume.
Causes:I) High output states- fever, anemia, pregnancy, Beri beri, thyrotoxicosis
II) Cardiac- AR, RSOV, PDA, AP window
5) Radioradial, radiofemoral delay & apex pulse deficit
Q-When can radiofemoral delay be appreciated?
A-If more than 40 millisec difference is present.
Q-What are the reasons of radioradial delay?
A-They are:
- SVAS,
- Coarctation aorta with involvement of SCA or with origin of the right SCA distal
to the coarct segment
- BT shunt- classic or rarely modified
Q-What is the normal time delay between the apex beat & a peripheral pulse?
A-The time difference normally between apex beat & a peripheral pulse is:
- Carotid artery= 30 millisec
- Brachial artery= 60 millisec
- Femoral artery= 75 millisec
- Radial artery= 80 millisec
JUGULAR VENOUS PULSE
Q-Why is JVP seen in the internal jugular vein?
A-It is easier to recognize pulsations in the EJV than IJV but still the EJV is not used as
an indicator of RA pressure due to:
1) Presence of valves in EJV
2) EJV passes thru’ more fascial planes & may be affected by extrinsic compression.
3) IJV is in a straight line with RA.
Q-Describe the technique of measurement of JVP?
A-Patient is kept in reclining position (at 45) & the neck is supported to relax neck
muscles (especially the sternomastoid)  normally 5-9 cm of H2O from the mid RA or
0-4 cm from the sternal angle of Louis (center of RA lies ≈ 5 cm below the sternal angle).
[Note:In a healthy individual, at an angle of 45, the mean level is invisible. However the
a & v waves will be visible just above the clavicle (sternal angle).]
Q-How to differentiate JVP with carotid pulse?
A-The JVP is characterized by:
- postural variation,
- decrease in impulses with inspiration &
- not palpable impulse/ pulse.

Q-Describe the components of normal JVP.
A-A normal JVP has:
‘a’ wave:
Due to Rt. Atrial contraction.
Normally ‘a’ is the largest positive wave.
‘a’ wave absent in- atrial fibrillation.
Tall ‘a’waves in- TS, tricuspid atresia, RA myxoma, pulmonary hypertension, PS with
intact IVS
Cannon ‘a’ waves incomplete heart block, when the RV contacts against a closed TV,
ectopic beats.
‘c’ wave:
Produced by;
1) impulse of carotid artery on adjacent veins,
2) bulging of the TV into the RA.
‘c’ is not normally seen & it merges with the ‘a’wave to form the and colleagues
complex.
‘x’descent:
Due to venous filling of the RA during which the RA is relaxed & TV is closed.
‘v’ wave:
Due to continuing RA filling against a closed TV.
‘v’waves are prominent in- TR, constrictive pericarditis.
‘y’ descent:
Due to the opening of the TV, corresponds to the S3.
Rapid y descent is seen in- TR, constrictive pericarditis
Slow y descent is seen in- TS
Q-How is a raised JVP, secondary to a cardiac cause, differentiated from an elevated JVP
due to SVC obstruction?
A-The JVP, which is raised in SVC obstruction, will show variation with respiration.
Q-What is Kussmauls sign?
A-Normally the JVP lowers during inspiration. But in constrictive pericarditis, there is an
increase in JVP on inspiration.
Q-Discuss Hepatojugular reflex.
A-Normally when sustained pressure is applied to the right hypochondrium, initially the
JVP rises due to increased hepatic venous return, but rapidly returns to normal.
But in overt CCF, continuous sustained pressure (30 sec) will keep the JVP persistently
high as the failing heart cannot compensate for the increased venous return. Removal of
pressure will lead to an abrupt fall by > 4 cm H2O.

BLOOD PRESSURE
Q-Describe the ‘cuff’ that is used to measure the BP.
A:
Name- Riva Rocci cuff
Optimum length of cuff- 2/3rd the circumference of the limb wih the center of the cuff
overlying the artery
Optimum width of cuff- 20% more than the diameter of the limb.
Normal width of cuff in adults is 12 cm for upper limb & 15 cm for lower limb
(if the width is narrower, a higher pressure will be recorded)
Q-How is lower limb BP measured?
A-For measurement of lower limb BP the patient lies prone & a 18 cm cuff is applied
above the level of the knee. Auscultation is carried out in the popliteal fossa.
Q-What are phases of Korotkoffs sound?
A-(from Hutchisons manual)
There are 5 phases:
1st phase- peak systolic pressure,
2nd & 3rd phase- due to turbulent blood flow thru’ a partially occluded artery.
4th phase- muffling of sound, & is 7-10 mm Hg above the true DBP.
5th phase- absent sound- true DBP.
Q-When is Korotkoff’s 4th phase used for measuring DBP?
A-In physiological conditions like pregnancy & pathological conditions like AR, PDA
and RASOV.
Q-What are the values of ‘normal’ BP in children?
A-A rough formula is as follows:
SBP= 90 + (age in years x 5)/ 2
DBP= 60 ± 20 m Hg
[Note:Normally the right UL BP is slightly higher than the left UL.]
Q-What conditions are associated with an abnormally high right UL BP?
A-The following conditions are associated with a abnormally high right uppel limb BP:
1) Interrupted arch
2) Supravalvar AS
3) Coarctation involving the left SCA.
Q-Does gravity affect BP?
A-For a distance above or below the level of the heart, subtract or add 0.77 mm Hg/cm.
Q-What is Ossler’s sign?
A-Ossler’s sign is pseudohypertension that is seen in Moenckbergs degeneration, where
the artery is sclerotic. Thus even with a lower systemic BP, the recording obtained is high
as the cuff is unable to occlude the artery (as it would normally do on inflation.)

CLUBBING
Definition: Bulbous enlargement of the soft parts of the terminal phalanges with both
horizontal & transverse curving of the nails.
Grades: 4 grades:
I) Softening of the nail bed
II) Obliteration of angle of nail bed
III) Increase in the curvature of nail- parrot beak/ drum stick appearance
IV) Swelling in all dimensions with X ray e/o subperiosteal new bone formation
(hypertrophic pulmonary osteoarthropathy)
Q-What are the theories of clubbing?
A-There is interstitial edema & dilatation of arterioles & capillaries due to:
1) Serotonin theory- increased fibrous tissue deposition
2) Hypoxia- stimulating opening of AV fistulae to increase blood flow to fingers &
toes
3) Reduced Ferritin in venous blood escapes oxygenation in the lung & enters
systemic circulation & acts as a stimulant for dilatation of AV anastomosis.
4) Neuronal theory
Q-What is Pseudoclubbing?
A-In hyperparathyroidism, resorption of bone leads to bulging of fingertips. However the
nail curvature is normal.
Q-What are the causes of clubbing?
A-The causes are:
1) Generalized clubbing:
i. Pulmonary- brochiectasis, lung abscess, bronchogenic carcinoma,
ii. Cardiac- cyanotic HD, Eisenmengerisation, infective endocarditis
iii. Alimentary- ulcerative colitis, crohns disease, cirrhosis
iv. Endocrine- myxedema, acromegaly
v. Others- idiopathic, hereditary
2) Only UL clubbing- IV drug abusers
3) Only LL clubbing - in farmers who work bare feet.
4) Unilateral limb clubbing - pancoast tumor, subclavian artery aneurysm
5) Unidigital clubbing - gout
Q-Which conditions are associated with clubbing but without cyanosis?
A-The following:
- Infective endocarditis
- Non cardiac etiologies

Q-What are the objective signs of clubbing?
A-
1) Schamroths window- normal diamond shaped space in between two approximated
nails. Lost in clubbing.
2) Distal phalyngeal depth > interphalyngeal depth. If more than 1, then clubbing is
advanced.
3) Lowibonds angle- acute angle formed by the nail bed. Disappears with clubbing.
CYANOSIS
Please see history proforma detail of cyanosis (page 19).
EDEMA FEET
*Location of edema in CCF depends upon the posture of the patient. In patients who are
mobile, the edema is checked by pressing against distal anterior tibia & fibula. In patients
who are recumbent, edema is checked over the sacrum & dorsal spine.
PALLOR
Q-Describe clinical estimation of hemoglobin.
A-Rough estimate of hemoglobin:
Palmar crease pale- Hb < 7 gm%
Venous hum- < 5 gm%
Functional PS- < 5 gm%.
ICTERUS
Q-Describe clinical estimation of jaundice.
A-A rough estimate of depth of jaundice:
Face > 5 gm% total bilirubin
Trunk> 10 gm%
Lower limbs> 20 gm%.

TUBERCULOSIS
Q-What are the peripheral signs of TB?
A-They are:
- lean thin individuals - phlyecten (medial)
- saddle nose - scars & sinuses on neck
- deformity of chest wall & spine - scrofuloderma
- lupus vulgaris - errhythema nodosum
- thickened spermatic cord
Q-What are the CVS manifestations of TB?
A-They maybe in form of:
1) Pericardial effusion
2) Constrictive pericarditis
3) IVS granulomatous lesion
4) Aortoarteritis (of aorta & rarely causing a PA aneurysm- called the Rasmusen’s
aneurysm).
PERIPHERAL SIGNS OF AR
Q-What are the peripheral signs of AR?
A-They are:
1) Wide pulse pressure.
- mild= 40- 60 mm Hg
- moderate= 60- 80 mm Hg
- severe= > 80 mm Hg
2) Hills sign- Difference between the systolic BP of LL & UL.
- mild AR= 20 –40 mm Hg difference
- moderate= 40- 60 mm Hg
- severe= > 60 mm Hg
Q-What is reason for a Hill’s sign?
A-Believed to be due to:
a) Impaired reading recording due to excessive muscle bulk of thigh thus
requiring higher pressure in the cuff to occlude the artery
b) Augmentation of the systolic wavefront by wave amplification, as the it
travels into the aorta to the periphery
3) Alfred de Musset sign (He was a poet)- increased pulsations of the head & neck
vessels.
4) Lighthouse sign- alternating blanching & perspiration of the forehead,
5) Landolfe’s sign- pupillary dilatation & contraction
6) Becker’s sign- Retinal artery pulsations.
7) Muller’s sign- pulsating uvula

8) Corigan’s sign- dancing carotids
9) Quinke’s sign- pulsatile capillary filling of nail bed on application of pressure over
the nails.
10) Waterhammer pulse- brisk upstroke, brisk downstroke with high volume, felt even
thru’ a less sensitive area like palm.
11) Locomotor brachials.
12) Mayne’s sign- < in DBP by > 15 mm Hg when BP is measured with arm hanging &
later with arm raised.
13) Austin Flint murmur- is due to:
a. Regurgitant jet hitting AML,
b. The coming together of 2 jets, ie, AR jet & The LA to LV jet, to
create turbulence,
c. Increased LVEDP
[Note:Even in severe AR an Austin Flint murmur may not be heard due to calcific AML
or an eccentric jet.]
14) Rosenbach sign- liver pulsations,
15) Gerhardt’s sign- splenic pulsations,
16) Duroziez murmur- on ausculatation over femoral artery, with pressure a systiloc
murmur heard distally & a diastolic murmur proximally
17) Lincoln sign- toe movements with cardiac contraction,
18) Traube’s sign- pistol shot femorals,
19) Shiley’s sign- Pulsating cervix.
MARFAN’S SYNDROME
Described in 1896 by Antine Marfan.
65-70% are by genetic transmission (caused due to mutation of the FBN1 gene on
chromosome 15.)
Q-What are the organ systems affected & diagnosis in Marfans?
A-The organ systems affected are CVS, Occular, pulmonary, skeletal & skin.
Diagnostic criteria laid down by Ghent:
1) Skeletal:
Major-
- Pectus escavatum/ carinatum
- Upper segment/ lower segment< 0.8
- Arm span/ height > 1.05
- Walker Murdoch sign (wrist sign)- little finger can go across the opposite wrist
and touch the thumb
- Steinberg sign (thumb sign)- thumb flexed and if it protrudes out of the medial
aspect of the hand, sign is +ve
- Metacarpal index> 8.4 (radiological length of 2,3,4 & 5 metacarpal added &
indexed to the added central diameter of the above metacarpals)
- Scoliosis
- Angle of elbow> 160º.

Minor-
- high arched palate- uvula not seen
- oblong head,
- endopthalmus
- down sloping eyes
2 major or 1 major + 2 minor criterion required for the skeletal system to qualify as a +ve
system.
2) Occular:
Major-
- subluxation of lens (mainly upward- characteristic feature of Marfans)
Minor-
- flat cornea
- axial length of globe > 23.5 mm,
- hypoplastic iris/ ciliary muscle
1 major or 2 minor criterion required for the occular system to qualify as a +ve system
3) CVS:
Major-
- dilatation of ascending aorta (> 40 mm) with/ without AR with dilated sinuses of
valsalva
- dissection of any portion of the aorta
Minor
- MVP with/ without MR
- Dilatation of MPA > 20 mm without peripheral PA stenosis, in age < 40 years.
1 major or 1 minor criterion required for the CVS system to qualify as a +ve system
4) Dura:
Major-
- lumbosacral dural ectasia
Minor- none
1 major criteria required for the dura system to qualify as a +ve system
5) Pulmonary:
Minor only-
- spontaneous pneumothorax
- blebs
6) Cutaneous:
Minor only-
- stretch marks
- spontaneous hernia

For the diagnosis of Marfans;
1) Genetic analysis +ve, 1 system +ve & one criteria of any other system, or
2) If genetic analysis not possible, then 2 systems should be +ve & 1 criteria from a
3rd system.
Q-At what age are the CVS manifestations of marfans generally seen?
A-Around 30 years of age. The other features can manifest at any age.
Q-In a patient with Marfans when is replacement of aortic root recommended?
A-If root > 40 mm, pregnancy not advised till root replacement.
If root > 45 mm, advised root replacement in all.
Q-What is the chance of transmission of Marfans to child.
A-50%.
FACIAL ABNORMALITY
Q-Describe characteristic facial abnormality that maybe seen in patients with heart
disease?
A-
- Elfine facies Williams syndrome
- Conotruncal facies AV cushion defects-TOF/ TGA/ DORV/ TA
- Downs syn Endocardial cushion defects
- Turners syn (slanting eyes Coarctation
micrognathia, web neck)
- Di Georges syn Truncus
(conotruncal facies)
- Noonans syn (hypertelorism PV dysplasia
low set ears, slanting eyes)
Q-When is the ear low set?
A-When a line is drawn from the outer canthus backwards, and it lies above the upper ear
helix.

CVS EXAMINATION
GENERAL PROFORMA
Inspection:
1) Chest- symmetery
2) Precordium
3) Apex impulse
4) Any other pulsations:
- parasternal
- suprasternal
- epigastric
- neck
- left 2nd ICS
5) Dilated veins
6) Scars & sinuses
7) Traile’s sign
Palpation:
1) Apex impulse
2) Diastolic shock
3) Thrill
4) Other pulsations
5) Trailes sign
Percussion:
1) Left heart border
2) Right heart border
3) Left 2nd ICS
Ausculatation:
1) S1
2) S2
3) S3/ S4
4) Murmurs
5) Other sounds

INSPECTION
PRECORDIUM:
Anterior aspect of the chest wall overlying the heart.
Normal precordium is smooth with same contour as the opposite chest wall.
Q-What are the causes of bulging precordium?
A-Is seen in:
- Cardiomegaly
- Pericardial effusion
- Mediastinal tumor
- Pleural effusion
- Chest wall deformity
Q-What are the causes of retracted precordium?
A-Is seen in:
- Fibrosis of lung
- Congenital chest wall deformity
APEX IMPULSE:
Lowermost & outermost area of the seen cardiac impulse.
Normally is in the left 5th ICS inside the midclavicular line.
Q-When is the apex impulse absent/ not seen?
A-It may not be seen in presence of:
- Pendulous breast
- Overlying rib (then turn the patient to left lateral decubitus & examine)
- Pleural effusion
- Emphysema
- Pericardial effusion/ constrictive pericarditis.
Q-What is the normal location of the apex impulse in children?
A-< 3-4 years of age the apex impulse lies in the left 4th ICS, in the midclavicular line.
Q-Which conditions are associated with ‘double apical impulse’?
A-Seen in:
- LV aneurysm
- HOCM
- Constrictive pericarditis
- Subaortic stenosis
Q-When is apical impulse considered diffuse?
A-If the impulse is > 1 ICS or > 5 cm diameter.

PULSATIONS:
A) Juxtaapical- seen in:
- Ventricular aneurysm
- HOCM
- Constrictive pericarditis
B) Epigastric- seen in:
- RVH
- Aneurysm aorta
- Hepatic pulsations
D/D between the above is by the 3-finger test.
C) Left 2nd ICS- seen in:
- Dilated PA
- Aneurysm aorta
- Enlarged LA
- L-posed aorta
D) Suprasternal- seen in:
- Arch aorta aneurysm
- AR
- Hyperkinetic state
E) On right side- seen in
- Dextrocardia
- Ascending aortic aneurysm
F) Back- seen in:
- Suzzmans sign for coarctation of aorta
G) Right sternoclavicular joint- seen in:
- Ascending aortic aneurysm
- Right sided aortic arch
H) In neck- seen in:
- AR
- Hyperkinetic state
DILATED VEINS OVER THE CHEST WALL:
Seen in:
- SVC/ IVC obstruction
- CCF
SCARS:
Of previous surgical procedure

PALPATION
APEX BEAT:
It is lowermost & outermost point where the cardiac impulse is felt.
It can be:
- heaving
- hyperdynamic
- tapping.
Q-Describe the characteristics of apex beat?
A-They are:
Normal- It is:
- localized to I ICS or < 2.5 cm diameter
- inside MCL
- lasting for < 50% systole
- felt as gentle tap
Tapping- Seen in RVH, It is:
- just a tap, not lifting finger
- localized
- only in early diastole
- no paramedical retraction
Hyperdynamic- Seen in LVVO (Eg. AR, PDA, MR), It is:
- diffuse, ie, > 2 ICS or > 5 cm diameter or > 2 finger width
- ill sustained (< 2/3 rd systole)
- outside MCL (generally)
- forcible
Heaving- Seen in LV pressure overload (Eg. AS), It is:
- diffuse,
- sustained (> 2/3 rd systole)
- forceful
PARASTERNAL HEAVE:
It is a systolic impulse felt in the left parasternal region due to:
- RVH
- Rarely due to aneurysmal descending aorta/ enlarged LA
Q-Describe grading of parasternal heave.
A-There is no grading of parasternal heave described. However a classification that may
be followed is:
- Grade I- gentle tap to the palpating hand (ulnar surface of hand)
- Grade II- lifts the hand but can be pressed by applying force to the hand
- Grade III- lifts the hand even on applying pressure
Q-What is Herztosis?
A-A highly pulsatile precordium is termed as Hertztosis. It is seen in chronic MR or
multivalvular regurgitant lesions.

TRACHEAL TUG (OLIVER’S SIGN)
Technique- Raise the chin of the patient→ apply firm pressure on both the sides of
cricoid cartilage with one hand (thumb & index finger) or 2 hands → a downward tug is
felt by the fingers with each heart beat. It is seen in- arch aneurysms & mediastinal
masses
DIASTOLIC SHOCK:
It is palpable 2nd heart sound.
THRILL:
It is a palpable murmur & feels like the purring of a cat.
[Note:Diastolic thrills are better felt than systolic.]
[Note:Thrill is present in stenotic lesions & absent in regurgitant (as the turbulence
produced by low flow is coarse).]
PERCUSSION
The finger should be placed along the length of the ICS. The static finger is the
pleximeter while the striking finger the flexiform.
Left border:
Technique: start from the 4th or 5th ICS in midaxillary line & come medially. The left
heart border should coincide with the apex.
If outside apex- consider pericardial effusion.
Upper border: for 2nd & 3rd space paramedially on the left side.
If dullness is present in the left 2nd / 3rd ICS anteriorly, the possibilities are-
- Pericardial effusion
- Aneurysm aorta
- Dilated PA
- L posed aorta
- Ductal ampulla aneurysm
Right heart border:
Technique: percuss in the midclavicular line till liver dullness → come one space
higher→ percuss medially till sternum.
Normally Rt. HB should be retrosternal. If dullness present, it may suggest:
- pericardial effusion
- right atrial enlrgement
- aneurysm ascending aorta
- dextrocardia

AUSCULTATION
The areas for auscultation are:
Mitral area Left 5th ICS inside the MCL
Tricuspid area Lower end of sternum
Aortic area 2nd right ICS
Erb’s area 3rd left ICS
Pulmonary area 2nd left ICS
1ST HEART SOUND:
Q-What are the causes of split 1st heart sound?
A-
- Electrical-
- RBBB
- VPB
- Mechanical-
- MS
- TS
- Myxoma
- Ebsteins
Q-What is a normal 1st heart sound?
A-A sound that is normal by character (no split) & intensity (experience).
Q-When is S1 considered loud?
A-When:
- louder than A2 at the apex
- equals/ louder than S2 at base.
Q-Why is the 1st heart sound split in Ebsteins?
A-Due to:
- RBBB
- RV dilatation
Q-What are the causes of a loud 1st heart sound?
A-S 1 maybe loud in:
1) Sinus tachycardia
2) Normally in children
3) High flow states- fever, anemia, pregnancy, thyrotoxicosis
4) Increased ventricular filling- MS, TS
5) Lt. To rt. Shunt- ASD, VSD, PDA
6) Short PR interval

Q-What are the causes for a soft 1st heart sound?
A-
1) Poor conduction of sound- thick chest wall, emphysema, pleural & pericardial
effusions.
2) MR, TR
3) Calcific MS
4) Long PR interval
[Note:S 1 is normally single & heard all over the precordium]
Q-What is the cause of a ‘reverse split’ of 1st heart sound?
A-Due to:
1) MS
2) LA myxoma
Q-Normally why does the MV close earlier than the TV?
A-Due to septal activation being from left to right.
SECOND HEART SOUND:
Normally A2 is audible in all areas while P2 is audible only in the pulmonary area & for
a short distance from the left sternal border.
Q-What is the normal splitting of S 2?
A-Normal spitting of the 2nd heart sound is:
During inspiration= 0.06 sec
During expiration= 0.02 sec
Q-When is P2 considered loud?
A-P2 is loud if:
- it is heard at the apex
- same or louder than A2 in the pulmonary area.
Q-When is A2 considered loud?
A-A2 is loud if:
- it is louder than P2 in the pulmonary area.
Q-What are the causes of a widely split S2?
A-The causes are:
-Electrical-
- RBBB
-Mechanical-
- ASD
- VSD
- PS
- RVF
- MR
- TAPVC

Q-What are the causes of a reverse split S2?
A-The causes are:
-Electrical-
- LBBB
- WPW syndrome
-Mechanical-
- AS
- PDA
- Coarctation
- Systemic HT
- LVF
Q-Enumerate causes of Single S2?
A-A single S2 maybe due to:
-A2 or P2 being soft
- AS
- PS
- TOF
-A2 & P2 summation
- VSD.PH
- Single ventricle
- Truncus
Q-What causes of Loud P2?
A-Pulmonary hypertension causes loud P2.
A rough estimate of PH can be obtained & is mentioned below.
If P2= A2 Mild PHT, PASP 30- 40 mm Hg
If P2> A2 moderate PHT, PASP 40- 75 mm Hg
A very loud P2 severe PHT, PASP > 75 mm Hg)
Q-What causes a loud A2?
A-Systemic hypertension causes loud A2.
Q-What is the movement of S2 split in relation to respiration?
A-During expiration, A2 & P2 nearly overlap. With inspiration, it is the P2 which moves
away. The A2 is fixed.
THIRD HEART SOUND:
Heard in the following conditions:
1) Normally till 30 years age
2) Normally in pregnancy
3) MR
4) TR
5) CCF
6) Myocardial infarction.

Q-What causes appearance of the 3rd & 4th heart sounds?
A-The 3rd & the 4th heart sound are due to abnormal filling patterns in the ventricles.
LVS3- during early rapid filling
LVS4- during atrial systole
FOURTH HEART SOUND:
*It represents a decreased compliance/ increased stiffness of the LV/RV.
*It is best heard with the bell of the stethescope with the patient in the left lateral
position.
MURMUR
Q-Describe the grading of murmur.
A-Grading of murmur was described by Levine & freeman in 1933.
I- III: are without thrill
IV- VI: are with thrill
Grade I: very faint murmur
Grade II: faint but easily audible
Grade III: loud without thrill
Grade IV: loud with thrill
Grade V: Louder, heard else where, with the side of the stethoscope placed sideways
Grade VI: Heard with the stethoscope lifted away from the chest wall.
[Note:Earlier the systolic murmurs were divided into 6 grades & the diastolic murmurs
into 4 grades]
Q-Which systolic murmurs are significant?
A-All systolic murmurs ≥ grade III are hemodynamically significant.
Q-Discuss murmurs in child.
A-Diastolic murmurs are always organic.
Systolic murmurs:
- Pansystolic- always organic; due to VSD, MR, TR
- Ejection systolic- organic if has associated
a. Symptoms
b. Cardiomegaly
c. > grade III
d. associated ejection click
Q-Describe the D/D between hypertensive PR Vs Normotensive PR.
A-
Hypertensive PR Normotensive PR
Murmur Decresendo Cresendo decresendo
P2 loud soft
RVH + -
Etiology All conditions with
increased PAP
APVS, post IE PV,
idiopathic dilatation of
PA, RVOT patch

Q-What are the causes of continuous murmur?
A-The causes are:
In a acyanotic:
1) PDA
2) AP window
3) RASOV into RA/ RV
4) Gerbodie defect
5) Coronary artery- RA fistula
6) Peripheral PS
7) ALCAPA
In a cyanotic:
1) With PDA
2) Bronchial collaterals
3) Pulmonary AV fistula
4) Surgically created shunts
Q-What is the D/D of apical murmur in CHD?
A-Apical murmur maybe due to:
1) ASD with MVP
2) Primum ASD
3) Ebsteins with c TGA
OTHER SOUNDS:
-Opening snap
Q-Besides MS, what are the other causes of an opening snap.
A-The possible causes maybe:
From the Mitral valve From the tricuspid valve
MR ASD
PDA TR
VSD Ebsteins.
Q-When is the characteristic of a continuous/ machinery murmur?
A-It crosses over the 2nd heart sound.

CARDIOPULMONARY BYPASS
Q-What should include a Prebypass checklist?
A-It should include:
- Occlusion
- Heparin
- ACT=__________
- Line pressure
- Cool to_____C
- Clamp off
- Anesthesia
- Bubble detector
Q-How are flow rates calculated on pump?
A-
= BSA x 2.5 L/ m2
< 7 Kg 120- 200 ml/ min
7- 10 Kg 100- 150 ml/ min
10- 20 Kg 80- 120 ml/ min
> 20 Kg 2.4 L/ min/ m2
All to maintain a mixed venous O% of 60- 70%
Q-What are the various levels of Hypothermia?
A-
Mild 32- 35C
Moderate 28- 32C
Severe 18- 28C
Profound 15-18C
Q-What are the considerations for conducting CPB during pregnancy?
A-The considerations are:
1) Avoid CPB, if possible (avoid the surgery)
2) If possible, perform during the 2nd trimester
3) Continuous fetal heart rate monitoring
4) Keep high flow rates (> 3 liters/ min/ m2)
5) Avoid acidosis & low PaO2
6) Maintain perfusion pressure above 65 mm Hg, for adequate blood flow to the
uterus
7) Low priming volume (for lesser hemodilution)
8) Hct > 22%
9) Turn patient to left (15- 20) to keep gravid uterus off the IVC
10) Do not cool
11) Restrict cardioplegia to minimum & aspirate away, if possible (to avoid
hyperkalemia)
12) Strict Act monitoring

13) Avoid alpha agonist
14) Avoid SNP (cyanide toxicity to fetus)
15) Administer tocolytics
Maternal mortality= 3%
Fetal mortality= 19%
Q-Can LMWH be administered in pregnancy?
A-No, as it crosses the placental barrier.
Q-What are normal blood volumes?
A-
Children= 85 ml/ Kg
Adults= 65 ml/ Kg
Q-How to calculate the amount of autologous blood to be removed?
A-
Volume to be removed= {Total bld volume x (Initial Hct- Desired Hct)}/ mean Hct
Q-How to calculate the amount of blood to be added?
A-
Volume of blood = [(Bv + Pv) x Desired Hct – Bv x Hct of patient]/ Hct donor blood
to be added (ml)
Bv= blood volume of patient
Pv= priming volume
Q-What is the height difference between the patient & the reservoir, during CPB?
A-It should be 25- 30 inches.
Q-What are the ways of confirming cardioplegia delivery?
A-Indicators of cardioplegia delivery are:
1) Aortic root distension
2) Heart stopping immediately
3) Generalized cooling of the myocardium
4) Coronary veins become bright red & distended
5) Blood returning from opposite coronary ostia if direct coronary injection being
given
Q-When does the myocardial activity continue even after delivery of cardioplegia?
A-The possibilities are:
1) Partially applied aortic clamp
2) AR
3) Incomplete venous drainage
4) K+ not added

Q-What are the types of pumps?
A-The pumps can be classified as:
Positive Displacement
- Roller
- Peristaltic (affinity)
- Blade
Centrifugal
- Vortex (Biopump)
- Impeller
o Radial
o Axial
o Mixed
Q-What are the specifications of the ‘Biopump’?
A-
Priming volume= 86 ml
Inlet/ outlet ID= 3/8 inch (9.5 mm)
Maximum operating pressure= 1100 mm Hg
Outer housing of polycarbonate
Q-What is secondary cardioplegia?
A-Is used when, due to poor myocardial protection, the patient cannot be weaned off
bypass. It comprises of high potassium, substrate enhanced cardioplegia administered
over 15- 20 minutes.
The benefits are:
1) Channelising post ischemic O2 uptake towards reparative processes rather than
wasting the aerobic energy towards needless electromechanical work
2) Restores synchronous contraction
Later the heart is allowed to beat empty for upto 30 minutes.
Q-What is ‘Kiss approach’ for open-heart surgery?
A-It was advocated by Victor Solomon. KISS stands for “Keep It Simple and Safe”.
Q-What are the reasons & management of High K+ on bypass?
A-Reasons are:
1) Suction hemolysis
2) Priming with banked blood
3) Small tip aortic cannula (hemolysis)
4) Prolonged CPB
Management includes:
1) Calcium
2) NaHCO3
3) Glucose insulin
4) Lasix

Q-What are the advantages of Mannitol during CPB?
A-Advantages are:
1) Cardioprotective/ neuroprotective
2) Renoprotective- increase urine formation
3) Maintains oncotic pressure
4) O2 free radical scavenger
Q-Based on O2 dissociation curve mention disadvantages of conventional cardioplegia?
A-They are:
1) Hypothermia- causes shift to left hence O2 is not easily released from Hb
2) Alkalosis- shift to left hence O2 is not easily released from Hb
These actions are negated by:
1) Tissue acidosis- shift to right hence O2 is released from Hb
2) Hypercarbia- shift to right hence O2 is released from Hb
Q-What is the importance of 2,3 DPG in cardiac surgery?
A- 2,3 DPG is low in banked blood  increased amount used  shift of curve to left 
less O2 available for tissues
Q-Why on bypass a high PaO2 is maintained?
A-A high PaO2 is required as on CPB the Hct is low. Hence for a higher O2 content of
blood a high high PaO2 has to be administered.
Q-What is Heparin rebound?
A-Post CPB, after neutralization of heparin with protamine, the heparin that is bound to
plasma proteins does not get neutralized. This is released later (after few hours) leading
to free heparin in blood.
Q-What is Pulmonoplegia?
A-Infusion of pulmonary artery with cold preservation solution prior to its procurement
for transplantation.
Q-What are the disadvantages of fibrillatory arrest?
A-It can cause subendocardial ischemia & necrosis.
Q-What is ‘electroplegia’?
A-For CABG on bypass- stimulate the vagus to arrest the heart transiently to enable a
stitch & then remove stimulus (experimental).
Q-What are the various counterpulsation techniques?
A-They are:
1) IABP
2) BASH (Body acceleration synchronous heart beat)
3) Pneumatic bandages over the body
4) Withdraw blood from one femoral artery during systole & inject into the other
during diastole.

Q-What is the concept of hemodilution?
A-It was introduced by By Zuhdi & Gott (1962)
Advantages of hemodilution are:
1) Decrease in viscosity leading to decreased SVR (hence increased perfusion) &
also requirements of lower flows
2) No use of blood products for prime- less chance of transmission of blood
mediated diseases, less load on the blood bank & for Jehovah’s witnesses
3) Increased urine formation
Q-What are absolute contraindications for retrograde cardioplegia?
A-They are:
1) Left SVC
2) Unroofed coronary sinus
Q-What is the amount of blood pushed, per revolution, thru’ the tubing used in CPB?
A-
3/8th tube= 22ml
1/4th tube= 12 ml
Q-Decsribe the causes of gas embolization during CPB?
A-Incidence= 1/ 8,000 open hearts
Causes are:
1) Inattention to level of oxygenator (generally seen after starting vasodilators.
Prevention- minimum level required for next 15 secs should be maintained. Use of
bubble detector, detecting bubble > 1cc )
2) Inadequate debubbling of the system before CPB
3) Poor surgical technique
4) Sudden return of cardiac activity
5) Break in the integrity of the oxygenator & connections
6) Clotted oxygenator
7) Air entry thru’ the cardioplegia line
8) Runaway pump
9) Reversal of the LV/ aortic vent
10) Rapid cooling & rewarming
Q-How to monitor gas emboli on CPB?
A-By using:
1) Infrared sensors on the arterial line
2) Carotid artery Doppler monitoring
Q-Ennumerate ways of preventing of air embolism?
A-Air embolism can be prevented by:
1) Attention to reservoir level
2) Light on arterial line
3) Arterial filter
4) Sensors on reservoir level/ arterial line

Q-What actions are to be taken if air has entered thru’ the arterial line?
A-The following actions are to be taken.
- Cooling of patient & administration of 100% oxygen
- Head low
- Increase depth of anesthesia with thiopentone
- Administer mannitol & corticosteroids
- Retrograde cerebral perfusion
Q-What are the problems of venting thru’ the aorta?
A-The problems are:
1) Faster rewarming (as blood passes thru’ the entire left side of heart)
2) LV distension possibility
3) Has to be stopped during cardioplegia
Q-When is definite indication of venting the PA?
A-RA myxoma.
Q-Enumerate techniques for achieving ‘pulsatile flow’ during CPB?
A-Techniques are:
1) Additional pump after oxygenator
2) IABP
3) After removal of cross clamp allowing the beating heart to be partially full
4) Changing revolution of pump constantly
[Note:Historical technique- Cross circulation]
Q-What are the various anomalies of coronary sinus?
A-They are:
1) Absent coronary sinus (left SVC into LA- Ragib’s defect)
2) Hypoplastic coronary sinus- some veins opening directly into RA
3) Atretic coronary sinus
4) Dilated coronary sinus
- without L-R shunt: Lt. SVC into coronary sinus
- with L-R shunt: intracardiac TAPVC
5) Unroofed coronary sinus
Q-Describe St. Thomas hospital cardioplegia solution.
A-
First described by Mark Brainbridge & Hearse.
St. Thomas I in 1975 & St. Thomas II in 1981.
(St. Thomas Hospital is in London.)

Composition is:
(All in per liter of solution)
St. Thomas 1
(Trade name: MacCarthy)
St. Thomas 2
(Trade name: Plegisol)
NaCl (mmol/L) 144 110
KCl (mmol/L) 20 16
MgCl 16 16
CaCl2 2.4 1.2
NaHCO3 - 10
Procaine 1.0 -
PH 5.5- 7.0 7.8
Osmolarity 300- 320 285- 300
St. Thomas 1 prepared by adding 1 ampoule (16 + 16 + 1) to 1 liter ringer lactate
Q-How much is the pressure with which the cardioplegia solution is pumped?
A-A maximum of 100 mm Hg difference between the pumphead & aorta.
Q-What happens if cardioplegia is administered at a high pressure?
A-It can result in rupture of capillaries & arterioles.
Q-What are the advantages of snugging SVC/ IVC on bypass?
A-The advantages are:
1) For RA/ RV surgery
2) During accidental opening of the RA during left sided surgery
3) Prevents early rewarming of the heart
Q-What is the pressure at which cardioplegia is delivered?
A-
Antegrade cardioplegia: 120 mm Hg- 1st cardioplegia
: 75 mm Hg- 2nd cardioplegia
Retrograde cardioplegia: 25 mm Hg
Q-Why is the LCA the first to be perfused during direct osteal cardioplegia delivery?
A-Because:
1) The LV will be arrested first
2) It is easily seen.
Q-How much the Hct is maintained on bypass?
A-Normally 20- 25%.
Lower Hct is required to be maintained with hypothermia
Mild  25% Hct
Moderate 22- 25% Hct
Severe 18- 22% Hct

Q-What is the Hct of cardioplegia?
A- 10%
Q-What are the advantages of blood in cardioplegia?
A-They are:
1) Acts as buffer
2) Has O2 carrying capacity
3) Provides substrates for metabolic demands of myocardium
4) Free O2 radical scavengers
5) Anti-edema action due to high colloid osmotic pressure
Q-What are the disadvantages of blood cardioplegia?
A-They are:
1) Increased viscosity, leading to stagnation
2) Shift of O2 dissociation curve to left, hence O2 not readily released
3) The high amount of O2 & substrates are not really required
Q-What are the various additives to cardioplegia?
A-They are mentioned below:
ADDITIVE FUNCTION
Potassium, Magnesium & procaine For immediate arrest
Hypothermia (10- 20C) For decreased metabolism
Glucose As substrate for metabolism
Oxygen/ blood Substrate
Glutamate & aspartate Substrate
Bicarbonate/ THAM/ phosphate Buffer (to provide optimum environment
for metabolism)
FFP/ albumin Colloid (provide osmotic pressure & hence
preventing cellular edema)
Mannitol For reducing edema
Methylprednisole For preventing edema
Q-What is normal heart O2 uptake & what is the concept of warm induction?
A-The heart uptakes O2 over time & not by dose. Hence during warm induction, it is
important to deliver the cardioplegia over a period of 5 minutes. This is followed by
delivery of cold cardioplegia over 3 minutes.
The strategy of warm induction is especially useful in energy-depleted hearts like;
- Cardiogenic shock
- Left main disease with unstable angina
- LVF
Q-What is the purpose of periodic cardioplegia?
A-It is for:
1) Maintaining arrest
2) Hypothermia
3) Buffer for acidosis

4) Provision of O2
5) Provide substrate
6) Wash out metabolites
7) Counteract tissue edema
Q-What are the types of membrane oxygenators?
A-They are:
1) Hollow fibre
- cross current
- counter current
2) silastic membrane
Q-Mention technicalities of the hollow fibre design.
A-
1) O2 flows thru’ the hollow fibres & blood from the outside
2) O2 depends upon the blender
3) CO2 diffusion is passive
4) The resistance to blood is high by the oxygenator, hence the pump is placed prior
to the oxygenator
5) Heat exchange is prior to oxygenator (blood passes over water filled coils)
Q-Mention technicalities of a silastic membrane design.
A-
1) An envelope of silicone rubber membrane is wrapped over a central spool. The O2
passes inside the envelope & the blood thru’ the windings.
2) Rest as with hollow fibre design (points 2- 5)
Q-What is the speed of cooling and rewarming during CPB?
A-Cooling occurs more rapidly than rewarming
0.1- 1.5C/ min Vs 0.3 – 0.5C/ min
Q-What is the temperature gradient between blood & water (heating bucket) during
rewarming & cooling?
A-It should be always  10C.
If it is more then:
- during fast cooling: when the cold blood reaches the patient O2, CO2. & nitrogen
will bubble out at the aortic end
- during rapid rewarming: when the warm blood reaches the heat exchanger,
bubbles will form.
Q-Mention specifications of arterial filters.
A-They are:
- 25-40 um
- at flow of 7 lit/min, gradient across filter is  30 mm Hg
-  200 ml is required for priming

Q-Provide brief description of ‘Cell savers’.
A-Introduced by Ansell (J Thorac Cardiovasc Surg, 1982)
Principle is as follows:
- blood sucked (by wall suction power)
- to this heparin added
- 20 um filter to remove clots/ debris
- RBC’s washed
- Centrifuge to concentrate
- Transfer to plastic bag for infusion
Q-Briefly describe total body retrograde perfusion?
A-First described by Yasuura, J Thorac Cardiovasc Surg 1994.
Total flow of 300- 500 ml/ min is administered at 13- 15C, at a pressure  30 mm Hg
Q-What is Post pericardiotomy syndrome?
A-It is seen 1- 2 weeks after CPB & lasts for 3- 5 weeks. It is characterised by fever,
malaise, leucocytosis, pericardial effusion, pericardial rub, and pleuritic chest pain.
It responds well to NSAID’s +/- steroids.
Etiology- not known (? Viral mediated)
Q-Discuss strategies for CPB induced complication.
A-The following are the strategies:
1) Heparin coated tubes to reduce blood activationby:
Heparin coating technique:
- Ionic bonds: Eg. Duraflo II (Baxter)
- Covalent bonding: heparin is attached to spacer arms (100 A long). Eq. Carmeda
(Medtronic)
2) Controlled activation of complements by
- Use of aprotinin
- Gp IIb/IIIa receptor antagonist to prevent platelet activation (experimental)
Q-What is reperfusion injury?
A-It is defined as, “the functional, metabolic & structural alterations caused by restoring
blood flow after a period of temporary ischemia.”
Pathophysiology: It is due to:
1) Intracellular calcium accumulation
2) O2 free radical release
3) No reflow phenomenon
4) Cellular edema
Q-How can reperfusion injury be avoided?
A-By providing an environment that is:
1) Hyperosmolar
2) Substrate enriched
3) Hypocalcemic
4) Contains O2 free radical scavenger

Q-What are the various sources of oxygen free radicals?
A-They are:
1) Lipid peroxidation
2) Neutrophil mitochondria (superoxide dismutase)
3) Conversion of hypoxanthine to xanthine
4) Arachidonic acid metabolism
5) Heber Wiess reaction
Q-What is ‘No reflow’ phenomenon?
A-It is a regional vascular occlusion, in the brain & probably other organs, leading to a no
reflow phenomenon after reperfusion of the tissues. Initially thought to be due to
hypothermia, but is now believed to be a response due to hypoxic endothelial cell
damage.
Q-What are intraoperative signs of inadequate myocardial protection?
A-They are:
1) Difficulty in defibrillating heart
2) Discoloration of heart
3) Poor contractility
4) Abnormal ECG;
- ST elevation
- Low voltage
- Wide QRS & loss of R
Q-What are the indication for topical cooling?
A-The indications are:
1) During AVR when RCA ostia is not present or cannot be perfused
2) Coronary artery disease with occluded RCA, where RV protection is not possible
3) Individual preference of surgeon.
Q-What are the disadvantages of topical cooling?
A-They are:
1) Phrenic nerve injury
2) If the heart is taken out of the pericardial well, for OM/ PD anastomosis: the
effect is lost
3) High incidence of atelectasis & pleural effusion
Q-Describe the protocol of Heparin administration for CPB.
A-Baseline ACT at incision
-300 IU/ Kg heparin (porcine or bovine) prior to cannulation
-add 2 U/ ml heparin to prime ( 5,000 U in adult)
-3 minute waitACTif > 300 secs CPB may be established
-if temperature< 30C- maintain ACT > 400 secs & if temperature < 24C- maintain
ACT > 500 secs
-if ACT < 300 secs after administration of upto 900 U/ Kg heparin, it is heprin resistance.
Administer 2 units FFP &/ or 1,000- 2,000 units AT III concentrate

Q-Describe Protamine administration protocol post CPB.
A-As follows:
-2-3 mg protamine per 100 U heparin administered
-Check ACT, if within 10 secs of post incision baseline ACT, there is no coagulopathy.
If more than 10 secs- suggests coagulopathy- add 25 mg more protamine
-Add 20 mg protamine for each 500 ml of heparinised pump blood.
-No protamine is required to cover cell saver blood.
Q-Is there any rate & site prefernce for protamine administration?
A-Recommended is a maximum of 5 mg/ min (in an adult) of protamine.
No difference has been noted on the site of administration, i.e., left or right
“It is the rate of administration & not the the site of administration”
Wakefield (Surgery, 1996) demonstrated a significant drop in the BP, HR & CoP with a
rapid administration of protamine to reverse heparin.
Q-What are the reasons for heparin rebound?
A-2 reasons are implicated
1) Release of heparin bound to plasma proteins
2) Release of heparin bound to endothelium
Maximum is within 1-3 hours, can appear as late as 6 hours.
It should be suspected if signs of bleeding appear after a period of dryness in the
operating field.
Q-Can LMWH be used for conducting CPB?
A-Yes. Disadvantages of LMWH for conducting CPB are:
- No effective dosage known
- Inadequate reversal with protamine
Q-Describe the protocol followed for using LMWH for CPB.
A-Anticoagulation protocol with LMWH is as follows (A. Carpentier)
- LMWH- 75 mg/ m2- IV bolus
(Additional 10 mg for every unit of blood added to the prime)
- If expected CPB < 60 minutes- monitor ACT
- If expected CPB > 60 minutes- monitor anti Xa activity
- If Anti Xa activity is > 1 IU/ml the proceed with aortic cannulation
- Repeat Anti Xa activity 1 hourly & if it is < 1.4 IU/ml, add 40 mg/m2 of LMWH
every 1 hour
Results with the above policy:
1) Protamine reversal was partial
2) Postoperative bleeding was more with LMWH
3) No effect on decreasing the requirements of blood or blood products (due to CPB
induced coagulopathy)
[Note:LMWH is used only if unfractionated heparin is contraindicated]

Q-What are the advantages of venting heart, during CPB?
A-They are:
1) Prevents LV distension
2) Decreases wall tension
3) Increased subendocardial blood flow
4) Maintains a dry field
Q-Discuss the pathophysiology of ‘ill effects’ of CPB.
A-Ill effects are due to:
1) Abnormal hemodynamics:
a) non pulsatile flow
b) decreased perfusion pressure
c) decreased colloid osmotic pressure
d) hypothermia
2) Adsorbed plasma proteins: viz. fibrinogen, albumin, Factor XII
3) Activation of blood constituents (most important mediator of morbidity due to
CPB). Blood constituents activated are
a) plasma protein systems, viz
i. contact system: Factor XII, Factor XI, prekallikrein, high
molecular weight kininogen
ii. intrinsic coagulation pathway (major stimulus for coagulation
during CPB)
iii. extrinsic coagulation pathway
iv. complement system
v. fibrinolytic system
b) blood cells, viz.
i. platelets
ii. neutrophils (mediate much of the inflammatory response due
to CPB)
iii. monocytes
iv. lymphocytes
v. endothelial cells
Q-What are the various emboli produced during CPB?
A-They are:
1) Fibrin
2) Platelet aggregates
3) Neutrophil RBC debris
4) Gaseous (nitrogen, oxygen)
5) Spallated material

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