1.

History and symptomatology

History proforma
 Demographic details
 HOPI
o Ask about all 5 cardinal symptoms
 Dyspnoea- onset, progression, duration, orthopnoea, PND, NYHA,
aggravating and relieving factors. Define daily physical activity
 Chest pain- site, onset, nature, radiation, aggravation and relieving
factors, duration, number of episodes
 Syncope- Onset, duration, consciousness and orientation before and
after the episode
 Palpitaitons- Exertional or at rest, regular or irregular, duration, NYHA,
fast or slow or increased force
 Pedal oedema- unilateral vs. bilateral, extending up to where
o Cough, haemoptysis,
o Symptoms of right heart failure- pedal oedema, ascites, decreased urine output,
right upper quadrant pain (congestive hepatomegaly)
o IE history- Fever
o Complications of IE- stroke/TIA, haematuria
 Past history
o Past h/o fever with joint pain- Rheumatic fever
o Cyanotic spells relieved by squatting if suspecting congenital heart disease
o Heart surgeries- IE
 Personal history
o IV drug abuse if suspecting IE

Cardinal symptoms- chest pain, dyspnoea, palpitations, syncope, oedema

Dyspnoea- Abnormal awareness of one’s own respiration (Dr. Hamide)
 Cardiac dyspnoea vs pulmonary dyspnoea- Cardiac dyspnoea is associated with
orthopnoea, PND and the other cardinal CVS symptoms.
 Orthopnoea mechanism- When the person moves to the supine position from the
standing position, there is increased venous return to the heart. When the LV cannot
handle this increased venous return, it causes backflow leading to pulmonary
venous congestion and dyspnoea.
 PND- due to interstitial fluid
 Orthopnoea more severe than PND
NYHA Grading (Dr. Hamide)- Can also be used for chest pain, palpitations
Class I- Dyspnoea with unaccustomed exercise
Class II- Dyspnoea with accustomed exercise
Class III- Dyspnoea with day to day activities
Class IV- Dyspnoea at rest

NYHA (Dr. Vivekanandan)

Class I- Ordinary physical activity does not produce dyspnoea
Class II- Ordinary physical activity produces dyspnoea
Class III- Less than ordinary physical activity produces dyspnoea
Class IV- At rest
 Problem- No definition of ordinary physical activity

Chest pain- Site, onset, character, radiation, associated with, timing, exacerbating and
relieving factors, severity
Oedema
 Location
 Duration
 Present until what level- like up to the thigh, knee etc
 u/l vs b/l-

 Relieving factors

Character Vasovagal Syncope Seizure

Trigger Typically present- illness, pain, Often none, but can be sleep
emotion deprivation, alcohol, drugs
Prodrome Feeling faint, tinnitus, nausea, Not always present.
dimming of vision
Duration of unconsciousness <60 seconds 1-2 minutes
Convulsion May occur but brief myoclonic Usually 1-2 minutes in tonic
jerks clonic
Colour Pale/grey Red/blue, may be pale
Lateral tongue biting Very rare (may bite tip) Common
Recovery Rapid, no confusion Gradual, over 30 minutes,
often confused, amnesic.

Canadian Cardiovascular Society Grading of Stable Angina

 Grade 1- Ordinary physical activity like walking and climbing stairs does not cause angina.
Angina with strenuous exercise only.

Grade 2- Slight limitation of ordinary activity.

Grade 3- Marked limitation of ordinary activity. Walking 1-2 blocks on the level or climbing
<1 flight of stairs.

Grade 4- Inability to carry out any physical activity without discomfort. May be present at
rest also.

Palpitations
 Defintion- Dr. Hamide
o Abnormal awareness of ones own heartbeat
 At rest- more likely due to arrhythmia
 Exertional- more likely due to a regurgitant lesion
 AR and MR will both have palpitations as a presenting complaint. In AR, dyspnoea
occurs much later than the palpitations, whereas in MR, they can occur at almost
the same time
Assessment of the history:

 Features suggestive of Left Heart failure- MI, Hypertension, Valvular heart disease,
myocarditis, Arrhythmias
 Features suggestive of Right Heart Failure- Cor pulmonale, ASD, Pulmonary stenosis
 Biventricular failure- High output states (esp Anaemia in failure), Left heart failure
 Global dysfunction- Cardiomyopathy, Myocarditis

2. Examination

General Examination

SIGNS OF IE AND RHEUMATIC ACTIVITY

Painless, pea sized nodules over bony prominences- extensor aspects of long bones
Swelling over joints
Signs of IE:

Osler Nodes, Janeway lesions, Splinter haemorrhages, Roth spots

 Janeway lesions- Nontender erythematous macules on the palms and soles
 Osler Nodes- Tender subcutaneous violaceous nodules mostly on the pads of the
fingers and toes
 Roth spots- exudative oedematous haemorrhagic lesions of the retina with pale
centres
 Splinter haemorrhages- non blanching reddish brown lesions under the nail bed
  Immunologic phenomena in IE- Osler nodes, Roth spots and microscopic haematuria

1. Vitals-
Temperature- measure with a thermometer. In CVS cases, raised temperature is expected to
cause tachycardia. If the Temperature is high but PR is low, it is known as inappropriate
bradycardia.
Pulse- Rate, Rhythm, Volume (only determined after pulse pressure), Character
Are all the peripheral pulses felt? Peripheral vascular disease, Pulseless diseases (Takayasu),
Coarctation of Aorta, Emboli
If the pulse is low volume and slow, it indicates a state of decreased cardiac output, possibly
due to valvular stenosis.
If in A. fib- check for apex-pulse deficit****
(Mechanism of apex-pulse deficit: Due to the irregular rhythm, there is variable durations of
diastole, so some ventricular contractions are strong and others are weak. The weak
ventricular contractions will cause a cardiac contraction but will not be strong enough to
cause a pulse)
Respiratory Rate-
Blood Pressure- Upper limb and Lower Limb
Wide pulse pressure is defined as PP > 60 mmHg. Caused by high output states.

2. Pallor- Along with pallor, check for ruddy conjunctiva/suffused conjunctiva. Indicates
polycythaemia which points to congenital cyanotic heart disease.
3. Icterus- better to avoid
4. Cyanosis- Ask the patient to stick out their tongue and leave it out for some time. Also check
the lips, nail bed, ear lobe, tip of the nose, inner surface of lips, palate for central vs.
peripheral cyanosis
5. Clubbing- Grading, pandigital vs. differential clubbing.
CVS causes of clubbing- Congential Cyanotic Heart Disease, Infective Endocarditis, Left Atrial
Myxoma
6. Oedema- Check for pitting on a bony prominence like shin of tibia / just above medial
malleolus
Slow oedema -pitting lasts >40 sec. Indicates sodium and water (4kg) retention in
extravascular compartment. Treatment is salt restriction.
Fast oedema- pitting <40 sec. Due to hypoproteinaemia.
Oedema in a cardiac patient is seen in presacral region- that is the dependent part.

Cardiac Examination

Inspection
 JVP
 Trachea
 Thyroid
 Precordial inspection
o Precordial bulge
o Apical impulse
 o Pulsations- suprasternal, parasternal, epigastric, neck, left 2nd ICS
o Dilated veins
o Scars, sinuses
 Palpation
o Apex beat
o Left parasternal heave
o Palpable P2
o Thrills
o Epigastric pulsations
 Auscultation (diastolic murmurs are not graded)
 Levine and Freeman’s grading of murmurs
o Grade I/VI- very soft, heard in optimal conditions
o Grade II/VI- faint murmur but clearly audible
o Grade III/VI- moderately loud murmur but no thrill
o Grade IV/VI- Loud murmur with thrill
o Grade V/VI- Louder with thrill and can be heard away from the affected site
o Grade VI/VI- Loud, with thrill, can be heard even with the stethoscope lifted
from the chest
o Classical description of each murmur****
 Mitral stenosis murmur- First heart sound is loud. Second heart
sound is normal. A high pitched opening snap is heard after the
second heart sound with the diaphragm of the stethoscope,
followed by a low pitched, rough, rumbling, mid diastolic murmur
with/without pre systolic accentuation best heard with the bell of
the stethoscope with the patient in left lateral position with breath
held in mid expiration
 Aortic stenosis- First and second heart sounds are head. A harsh
crescendo-decrescendo type of ejection systolic murmur Grade___
is heard in the aortic area. It is best heard with the patient in the
sitting position while leaning forward, during expiration, with the
diaphragm of the stethoscope
 Mitral regurgitation- First and second heart sounds are not audible.
A high pitched loud pan systolic murmur of soft blowing (??) quality,
grade ___ is heard best with the diaphragm of the stethoscope,
radiating to the axilla
 Aortic regurgitation- First heart sound is heard. Second heart sound
is soft. A soft, high-pitched, blowing, decrescendo type of early
diastolic murmur best heard with the patient sitting and leaning
forward with breath held in expiration
 JVP- __ cm above the sternal angle. <4cm at 45° elevation is normal (MacLeod)
 If JVP is not visible/not raised but you are still suspecting Right Heart Failure, check
for abdominojugular reflux. It is a sign of incipient RHF.
 Visible pulsations in the neck?
 Trachea in midline?
  Thyroid enlargement? AF, Tachycardia, MR, TR
(Remember the carotid pulsations are of the common carotid artery)

DIAGNOSIS
1. Etiology- RHD/congenital
2. Valve and lesion- Ex: Mitral stenosis
3. Rhythm- Sinus/AF
4. Failure?
5. PAH?
6. Evidence of rheumatic activity/IE?

Notes:

Symptomatology

1. Chest pain
 Walk through angina- peripheral vasodilation during exercise relieves the symptoms
due to decreased myocardial workload
 Silent MI- pain is absent in 30% of patients with MI, especially in the elderly and
patients with DM.
 Anginal chest pain: Ache or dull discomfort, felt diffusely in the centre of the
anterior chest wall, lasting <10 minutes. Not affected by inspiration. Can have
triggers. Relieved by rest and GTN.
o Unstable angina- angina of abrupt onset or of increasing severity, duration,
frequency. May occur with minimal exertion or at rest.
o Crescendo angina- Increasing frequency at lower workloads, but not at rest.
o Nocturnal/decubitus angina- indicates severe coronary artery disease.
 MI: Prolonged anginal symptoms. May be associated with autonomic symptoms,
especially in inferior wall MI.
 Pericarditis: Sharp chest pain exacerbated by inspiration.
 Dissection: Abrupt onset of very severe, tearing chest pain that can radiate to the
back and is often associated with profound autonomic symptoms.
 Angina equivalent- symptoms of myocardial ischaemia other than chest pain like
dyspnoea, fatigue, syncope that are relieved by NTG
 Second wind angina- Occurs on initial exertion but then subsides only to recur on
subsequent exertion

Causes of chest pain

 Cardiovascular causes-
o Ischaemic causes- Angina, MI, IHD
o Non Ischaemic causes- Pericarditis, Aortic dissection, Pulmonary embolism,
Pulmonary hypertension, Aortic stenosis (because of LV hypertrophy, the
oxygen demand cannot be met), Aortic regurgitation (coronaries receive
 their blood supply in diastole which is when the regurgitation occurs),
HOCM (same as AS)
 Respiratory causes- Pneumonia, pneumothorax, pleuritis
 Gastrointestinal causes: Oesophageal spasm, Oesophageal reflux, Peptic ulcer
 Musculoskeletal causes: Costochondritis, Trauma, Cervical disk disease
 Psychological: Emotional and psychiatric conditions.

Dyspnoea
 Trepopnoea- dyspnoea in right or left decubitus position- seen in dilated
cardiomyopathy
 Platypnoea/orthodeoxia- dyspnoea/hypoxia (respectively) in the upright position
o LA thrombus
o LA myxoma
o Hepatopulmonary syndrome
o ASD- due to increased right to left shunting while standing up
o Pulmonary diseases with VQ mismatch
 Orthodeoxia
Syncope
o Definition- transient loss in consciousness due to cerebral hypopefusion
o Causes
o Cardiac
 Electrical anomalies- Bradycardia, heart block, ventricular or supra-
ventricular tachycardias
 Mechanical causes- AS, HOCM, Pulmonary stenosis, TOF, Pulmonary
embolism, LA myxoma (postural syncope)
o Hypovolaemia- haemorrhage, fluid loss etc
o Vasovagal syncope
 Characteristically occurs in response to fear, sudden emotional
stress, anxiety, anaemia etc
 Always preceded by warning symptoms like nausea, weakness,
blurred vision, headache
o Orthostatic hypotension
 Decrease in SBP by >20mmHg or DBP by >10mmHg within 3 minutes
of standing from the sitting position
 Causes- drugs (anithypertensives), diabetic autonomic neuropathy,
anaemia
o Post-tussive syncope- typically occurs in the setting of lung disease. Violent
coughing results in a decreased venous return due to raised intra thoracic
pressure
o Micturition syncope
Palpitations
o Abnormal awareness of one’s own heartbeat
o Causes- Dr. Hamide***
o Mechanical- due to volume overload- AR, MR, Thyrotoxicosis, PDA, Severe
anaemia etc.
o Electrical- Arrhythmias
Abnormal pulses:
  Definition of pulse**: Waveform felt by the finger that is produced by cardiac
systole which traverses the arterial tree in a peripheral direction
 Character of pulse is always assessed in carotid- because it is closer to aorta so the
character of the pulse is better transmitted
Normal pulse: Systolic and diastolic wave separated by a dicrotic notch which corresponds
to S₂ (closure of the semilunar valves)
Pulsus bisferiens: Two palpable systolic peaks of equal strength.
o When there is an ejection of a rapid jet of blood through the aortic valve, Bernoulli
effect (lateral pressure is inversely proportional to the velocity of flow through a
tube) comes into play on the walls of the ascending aorta causing a sudden decrease
in lateral pressure on the inner aspect of the wall.
o Causes-
o (Moderate)AS with (Severe)AR- The moderate AS causes a jet with extra
velocity to be shot out.
o HOCM- The obstruction occurs later in systole as the mitral valve begins to
approximate the hypertrophied septal area. There is a sharp drop in
pressure followed by a secondary rise to overcome the obstruction.
o Severe AR

Can also be detected as double Korotkoff sounds and Traube’s femoral sounds.

Bounding pulse
o Rapid rate of rise and large pulse volume
 o AR, PDA, Hyperthyroidism, Severe anaemia

Corrigan/Waterhammer pulse
o Exaggerated form of bounding pulse.
o Sudden, forceful, jerky rise is due to rapid filling of the radial artery
o When we raise the hand, gravity empties the radial artery. This further raises the
pulse pressure. Also, the radial artery comes into line with the aorta which makes it
sensitive to pressure changes in the aorta.
o The sudden, forceful, jerky rise is due to rapid filling of the radial artery caused by an
extra large amount of blood pushed by the distended LV into a relatively empty
vessel
o The collapsing character or sudden downstroke is partially due to sudden fall of
blood pressure in the aorta during diastolic regurgitation and partially due to rapid
emptying of the arterial system because of increased velocity of the blood stream.
o Causes- AR, PDA, other hyperdynamic circulatory states
Dicrotic pulse:
o Double peaked pulse, but the second peak arises from diastole.
o Suggests low cardiac output and increased systemic vascular resistance.
o Cause- LV failure

Pulsus parvus
o Low amplitude pulse
o Encountered in states of low cardiac output
Pulsus parvus et tardus: Rises slowly to a decreased peak. Characteristic of AS.

Bifid pulse: Classic pulse of HOCM. Appears as a ‘spike and dome’. Early systolic emptying ->
obstruction -> late systolic emptying
Bigeminy
Trigeminy
Pulsus paradoxus
o In normal individuals, the maximum drop in systolic BP with deep inspiration is <10
mmHg
o Mechanisms there for normal drop in SBP with inspiration
o Inspiration increases venous return due to negative intrathoracic pressure.
This increases RV filling which pushes the interventricular septum towards
the LV and decreases LV volume
o Increased venous pooling in the lungs which reduces LA filling
o If the SBP drops by >10mmHg, it is an exaggerated pulsus paradoxus
o How to measure pulsus paradoxus?
o Inflate the BP cuff above systolic pressure
o The pressure at which Korotkoff sounds are heard only in expiration is the
upper limit and the pressure at which Korotkoff sounds are heard in
inspiration and expiration is the lower limit. The difference is pulsus
paradoxus.
o Causes
o Cardiac tamponade- In tamponade, the pressure of the pericardium
increases markedly. So, when all the chambers attempt to relax, the
 pressure they can drop to is that of the pericardium. Hence diastolic
pressures in the right and left chambers are equal to each other. So,
increase in right heart filling during inspiration can only be accommodated
by bowing of the intraventricular septum towards the LV.
o Constrictive pericarditis- Normally, the pericardial and pleural pressures fall
by approximately the same amount during inspiration. But in constrictive
pericarditis, the thickened pericardium prevents the decrease in pleural
pressure from being transmitted to the cardiac chambers. So, the inspiratory
fall in in left sided filling pressures is absent or blunted. The pulmonary veins
are intrapleural but extrapericardial, so their pressure falls, thus the normal
gradient for LA filling is diminished, LV volume decreases and BP decreases.
o Asthma and COPD- Expiration raises the intrathoracic pressure by a
significant amount to overcome obstruction, so inspiration appears to lower
the systolic pressure excessively.
o Obstructive sleep apnoea and obesity- same mechanism as above.
o Reversed pulsus paradoxus- Inspiratory rise in arterial systolic and diastolic
pressure. Seen in HOCM because of decrease in LV volume on expiration
Pulsus alternans: Alternate strong and weak pulses despite normal rate and rhythm. Sign of
LV dysfunction. Most accepted theory- intermittent release of Ca+2 ions from the myocardial
sarcoplasmic reticulum. Pulsus alternans of >10 mmHg can be detected. Raise the BP cuff to
a pressure where no Korotkoff sounds are heard, then decrease until only one set is heard

 Normal pulse rate: 60-100/min

 Bradycardia: <60/min
o Causes
 Physiological- athletes (due to increased vagal tone), sleep
 Pathological
 Hypothyroidism
 AV block and other bradyarrhythmias
 Infectious bradycardia- Enteric fever, brucellosis,
Leptospirosis, Dengue
 Drugs- Beta blockers, CCBs, Digoxin
 Hypothermia
 Tachycardia: >100/min
 Regularity of tachycardia
o Regularly irregular- bigeminy or trigeminy
o Regularly regular tachycardia- sinus tachycardia, ventricular tachycardia,
atrial flutter, paroxysmal atrial tachycardia
o Irregularly irregular- atrial fibrillation
o How to differentiate?
 V tach- usually unchanged by vagal manoeuvres. Findings of A-V
dissociation like cannon A waves and variable intensity of S1
 Paroxysmal atrial tachycardia- resolves abruptly after
Valsalva/carotid artery massage. Typically associated with a
pounding feeling in the neck due to simultaneous carotid pulsations
and cannon A waves
 Delays
o Tell only Radiofemoral delay
 o Cause- Coarctation of aorta, Takayasu, Atherosclerosis
o How to check?
 Normally, femoral pulse precedes radial pulse by a few milliseconds
 If radial precedes femoral, it is called radiofemoral delay
 Volume-
o Normal pulse volume means pulse pressure is 30-60mmHg
o Low pulse pressure- shock, MS, AS, cardiac failure
o High pulse pressure- Thyrotoxicosis, severe anaemia, Beriberi, AV fistula

JVP
Definition of JVP***- Jugular venous pressure is expressed as the vertical height from the
sternal angle to the zone of transition of distended and collapsed internal jugular veins
Jugular venous pulse is the reflection of the phasic pressure changes in the right atrium
 How to get right atrial pressure from JVP?
o Add height of JVP from sternal angle to 5cm (distance from RA to sternal
angle)
o Multiply that height by 0.736 to get mmHg RAP
o Normal value of RAP <6mmHg or <8cm blood

JVP vs. Carotid (POLICE)

Palpation- non palpable
Occlusion- readily occludable
Location- between the heads of SCM, lateral to carotid
Inspiration- drops with inspiration
Contour- biphasic wave form
Erection- drops when sitting erect

Internal jugulars vs External jugulars

 Internal jugulars are in direct straight line communication with the SVC which in turn
directly communicates with the right atrium, whereas the external jugulars
communicate with the SVC after two near 90° turns
 The external jugulars run through fascial planes, so they can get compressed
 The external jugulars can become invisible if constricted due to shock/heart failure
due to sympathetic stimulation (if their diameter was narrow to start with)
 However, the internal jugulars are never visible (except in severe TR). Their
pulsations are transmitted to the skin and are visible.
 The right internal jugular vein is preferred to left internal jugular vein because sometimes in
severely arteriosclerotic patients, the left innominate vein can get compressed between the
sternum and arteries arising from the aortic arch and cause falsely elevated JVP
 First check the JVP in the sitting position- if it is above the clavicle then check in other
positions
 Why do we see at 45° and not supine? Because in the supine position, the highest level of
JVP may be somewhere difficult to detect ???
 Why does it drop on inspiration? Because the drop in intrathoracic pressure causes a suction
effect
 However, the pulsations of JVP become more prominent on inspiration because the
increased venous return increases the volume of the right heart.
 Reduced JVP is seen in hypovolaemia.
 In bronchial asthma and emphysema, there is a wide variation of intrathoracic pressure with

respiration, so the JVP varies with respiration

 Waves (ACXVY)
a wave- Atrial contraction
c wave- TriCuspid valve bulging into RA, so isovolumetric contraction
v wave- venous return
x descent- Atrial RelaXation
Actually comprises x descent and x’ descent. X’ descent is between a and c and is
due to atrial relaxation. When the ventricles contract in systole, they pull the tricuspid valve
apparatus towards the apex, which increases the right atrial volume, causing a decrease in
right atrial pressure, represented by the X descent.
Y descent- atrial emptying
(A small component of the c wave is produced by carotid pulsations, hence called c wave)

Abnormalities of the a wave

 Prominent a waves- seen in causes of right ventricular hypertrophy- pulmonary
hypertension, pulmonary embolism causing acute cor pulmonale, pulmonic stenosis
 Giant a waves- Right atrium contracting against a stenosed tricuspid valve- tricuspid stenosis
 Cannon a waves- Right atrium contracting against a closed valve
o Intermittent cannon waves- AV dissociation (third degree heart block)
o Regular cannon waves- In junctional tachycardia. The focus is at the AV node. The
depolarisation spreads equally to the right and left chambers at the same time.
o In ventricular tachycardia, there is complete V-A dissociation, so there will also be
cannon a waves (important point to differentiate VT and SVT with aberrancy. In SVT
with aberrancy, as long as there is no third degree heart block, there will be AV
association, so no cannon a waves)
 Normally, the a wave has a higher amplitude than the v wave because the a wave is
produced due to active atrial contraction, while the v wave is produced due to passive atrial
filling. However, in the left atrium, the 4 pulmonary veins entry point decreases the
compliance of the left atrium, so it cannot generate as much pressure. In the left atrial wave
forms, a and v wave have similar amplitude. In ASD, left atrialisation of the jugular venous
forms occurs and a and v waves can have similar amplitude.

 Giant a waves can also be seen in marked LVH because the RV septum is pushed towards the
right, making RV filling more difficult (Bernheim effect)
 Cannon a wave differs from prominent a wave in that it begins just after S1 because it
represents atrial contraction against a closed tricuspid valve. It is the hallmark of A-V
dissociation. Giant a wave begins just before S1.
 Intermittent cannon a wave (Dr. Hamide)- Seen in complete AV block
 Regular cannon a wave (Dr. Hamide- Seen in junctional rhythm (the rhythm arises at or near
the AV node), sometimes SVT and VT
 Equally prominent a and v waves-RV failure, ASD (The V wave in LA is transmitted to LA)
 Prominent x descent- seen in patients with vigorous RV contractions, thus requiring strong
atrial contractions (like tamponade, RV overload)
 Diminished x decent- A fib, cardiomyopathy
 Prominent y descent- constrictive pericarditis, restrictive cardiomyopathy
 Diminished to absent y descent- TS
Tricuspid stenosis: TS is a diastolic pathology, so a wave and y descent are affected. A wave will be
giant because of increased right atrial pressure, and y descent will be diminished because RA
emptying is impaired.

Tricuspid regurgitation: In TR, the right ventricle pumps blood into the right atrium which increases
its pressure and thus prevents the decrease in pressure that causes a normal x descent. So x descent
is blunted.

PAY TAX- Pericarditis prominent y descent , Tamponade prominent x descent

Cardiac tamponade
 There is impaired RV filling due to fluid surrounding the RV- blunted y descent
 When the RV contracts, it makes room for the fluid to come to the RV and allows the RA to
get more space to relax- so prominent x descent.

Constrictive pericarditis
 The pericardium is stuck like an adhesive to the RV
 The RV relaxes very quickly which causes a rapid pressure drop, but its pressure increases
immediately due to a recoil of sorts
 This causes rapid y descent
 It also accounts for the “dip and square root” sign on cardiac catheterisation

Character Tamponade Constrictive Restrictive

pericarditis Cardiomyopathy
Kussmaul sign Absent Present Present
Pulsus paradoxus Present Present Absent
JVP Prominent x descent Rapid y descent
with blunted y
descent

Abdominojugular reflux
 Abdominal compression should make the JVP fall normally because pressure on the
abdomen obstructs femoral venous return so less blood reaches the RA
 In RV failure, the RA and RV have increased pressure. RUQ compression transmits increased
pressure to these chambers which already have high pressure, so the RV output decreases
and JVP will be raised for a sustained duration.
 Used to unmask subclinical RV failure and to confirm symptomatic LV failure.
 Apply your hand over the periumbilical area with fingers widely spread. Apply gradual, firm,
inward, steady pressure for at least 15 seconds.
Considered to be positive if JVP rises by >3cm throughout the compression.

Kussmaul’s sign
o Inspiration raises the intra-abdominal pressures and can thus produce effects similar
to abdominal compression, especially in patients with already raised right chamber
pressures
o Kussmaul sign is paradoxical rise in JVP with inspiration
o Normal fall of JVP on inspiration is 3 mmHg (not cm of water)
 o Seen in
oRight ventricular MI- tell this first
oRV failure
oTricuspid stenosis- due to backflow from RA
oCor pulmonale- due to RV failure
oConstrictive pericarditis- Right atrial pressure increases with inspiration but
it is not transmitted to the RV
o Restrictive cardiomyopathy- due to diastolic dysfunction
o Why not in tamponade?
o In tamponade, the RV can accommodate the increased venous return by
pushing the IV septum towards the LV. So, there is no Kussmaul sign, but
there is pulsus paradoxus because of decreased LV volume
 Bilateral elevated JVP without pulsation- SVC obstruction
 Unilateral non pulsatile elevated JVP- innominate vein or thrombosis
Heart sounds and murmurs

S1
 Cause- Closure of mitral and tricuspid valves at the end of systole. The mitral valve closes
when the LV pressure rises above the LA pressure
 Loud S1
o Mitral stenosis- Because of the increased Atrioventricular pressure gradient at the
onset of systole, there is an increased closing excursion of the mitral valve leaflets.

o Hyperdynamic circulatory states

o Holosystolic MVP with MR- the prolapse delays the tension of the leaflet, thus
allowing it to close at the peak of ventricular contraction
o LA myxoma- the tumour delays the closure of the valve
o Short PR interval
 P represents atrial contraction, and R represents ventricular contraction.
 If the PR interval is short, the ventricular contraction occurs so quickly after
the atrium has contracted that the LA has not had enough time to relax
(short x descent).
 Therefore, atrial pressure is still at a high level when pressure in the LV
exceeds it enough to close the mitral valve. The LV pressure has to reach a
higher level, which corresponds to a higher slope on the dP/dT curve which
causes a loud S1
o Ebstein anomaly- atrialisation of the RV. Loud S1 is because the malformed tricuspid
valve closes relatively late at a higher RV pressure.
 Soft S1
o Calcific mitral stenosis
o MR
o Long PR interval
o TR
o Acute AR
 Split S1
o Normally M1 is just 20-30 msec before T1
 o In RBBB, T1 can be heard much after M1
o Ebstein’s anomaly has associated RBBB
S2 split and its anomalies

1. Normal split- seen in inspiration. Normal duration is <0.03 seconds

2. Wide split
a. Wide variable split- VSD and MR (due to early A2), PS due to delayed P2
b. Wide fixed split- ASD, TAPVC, RBBB
3. Paradoxical split- seen in conditions that delay LV emptying like AS, LBBB

 Wide fixed split

o ASD
 Widely split- because of increased pulmonary hangout interval (interval
between the crossing over of the pressure between RV and PA and the
closure of the pulmonary valve) which leads to prolonged RV ejection when
the pulmonary valve is supposed to theoretically close. The increased
hangout interval is because the resistance of the pulmonary circulation is
low, so it takes some time for blood flow to completely cease. Aortic valve
does not have a hangout interval because the systemic resistance is very
high compared to the pulmonary resistance so blood flow stops very early.
 Fixed split because inspiratory increase in venous return is matched by
reciprocal changes in the volume of the left to right shunt, thus minimising
the contribution of respiratory variations to RV filling (Ref-Perloff’s physical
examination of the heart and circulation)
 o Total anomalous pulmonary venous connections- one or more pulmonary veins are
connected to the right atrium. This has an effect similar to that of ASD.
o Massive acute pulmonary embolism
 Soft A2- Aortic stenosis
 Soft P2- Pulmonary stenosis
 Loud A2- systemic hypertension, aortic aneurysm
 Loud P2- Pulmonary hypertension, pulmonary artery dilation

S3
 Cause- Initial passive filling of the ventricles in diastole
 Physiological S3
o Children
o Athletes
o Pregnancy
 Pathological S3
o MR, TR- because of increased volume in the atria that is filling the ventricles
o High output states
o Congenital heart disease- ASD, VSD, PDA
o HOCM
o Systemic and pulmonary hypertension

S4
 Due to emptying of atria into a stiff (non-compliant) ventricle
 Causes
o Systemic hypertension
o Coronary artery disease
o Severe Aortic stenosis
o HOCM
o Restrictive cardiomyopathy

Added sounds
 S3, S4
 Opening snap
o Produced due to the opening of AV valves
o Causes- MS, TS,
o Mechanism in MS- elevated left atrial pressure causes sudden opening of a stenotic
valve
 Ejection click-
o Produced due to opening of semilunar valves
o Pulmonary ejection click increases with inspiration. Aortic ejection click does not
have any change with respiration and is heard all over the precordium
 Pericardial knock- loud high frequency diastolic sound heard due to abrupt halt to early
diastolic filling in constrictive pericarditis
 Pericardial rub- sounds heard due to friction between the two layers of pericardium. They
can be pre-systolic, mid-systolic or mid-diastolic
 Tumour plop- diastolic sound heard in mobile LA myxomas
 Prosthetic sound
Innocent/functional murmurs
 Primarily physiological
  How to differentiate from a pathological murmur?
o Soft, less than 3/6 intensity
o Often position-dependent
o No symptoms
o Occur either during systole or continuously during systole and diastole. Any pure
diastolic murmur is pathological
o No palpable thrill
 Still’s Murmur- Inferior aspect of lower left sternal border, ejection systolic click, musical in
quality
 Venous hum- Infraclavicular, throughout the cardiac cycle
 Mammary souffle

Features of pulmonary hypertension

 Normal pulmonary arterial pressure: 15-25/10 mmHg
 Pulmonary hypertension definition- mean pulmonary pressure >25mmHg at rest or
>30mmHg after exercise
 Symptoms
o Breathlessness- often severe, exertional
o Easy fatiguability
o Dizziness
o Syncope
 Signs***
o Pulse- low volume due to decreased CO
o JVP- prominent a wave
o Inspection
 Visible pulmonary arterial pulsation in 2nd ICS
 Epigastric pulsation
o Palpation
 Apex goes outwards
 Palpable P2- diastolic shock
 Left parasternal heave
 Palpable P2
o Percussion- Left 2nd ICS is dull
o Auscultation- classical sequence of events
 Audible S1
 Pulmonary ejection click
 Pulmonary ESM due to relative PS
 Loud P2 with narrow S2 split
 Graham steel murmur
 Right sided S3

Effect of manoeuvres
Note: mitral valve is in the /\ orientation at low ventricular volume which is conducive for
early prolapse. At higher ventricular volumes, the orientation of the valve is more like __ __
which takes more time to prolapse.
 Inspiration increases all right sided murmurs except pulmonic ejection- Carvallo’s sign
 Sustained handgrip (increases afterload)
o Increases intensity of MR, AR, VSD murmurs
o Decreases HOCM and AS murmurs (because of increased LV volume)
 o Later onset of click/murmur in MVP
 Valsalva and standing (decreased preload)
o Decreases intensity of most murmurs including AS
o Increases intensity of HOCM murmur
o Earlier onset of click/murmur in MVP
 Rapid squatting (increased VR, preload, afterload)
o Decreases intensity of HOCM murmur
o Increases intensity of MS, AR, VSD murmurs
o Later onset of click/murmur in MVP.
o

Named murmurs****
 Austin Flint Murmur: mid diastolic murmur heard over the apex in severe AR. Believed to be
due to vibration of the anterior mitral valve leaflet due to the regurgitant jet
 Carey-Coombs Murmur: Mitral valvulitis associated with acute rheumatic fever can cause an
MDM audible at apex.
 Cole-Cecil murmur: early diastolic murmur of AR heard at apex or axilla
 Cruveilhier-Baumgarten Murmur: Venous hum heard in epigastric region due to collaterals
between the portal system and the remnant of the umbilical vein in portal hypertension
 Gibson Murmur: Machinery murmur of PDA
 Graham Steell’s Mumur: Murmur of pulmonary regurgitation (EDM)
 Means-Lerman scratch murmur: Increased flow across the pulmonary valve in thyrotoxicosis
may be associated with an ESM
 Roger’s murmur: PSM of VSD best heard at the left sternal border
 Seagull murmur: Murmur with musical qualities occasionally heard in AR. Can also be a sign
of tight calcific AS in Gallavardin phenomenon.
 Still’s murmur: Innocent(benign/physiological) murmur resembling the noise of a twanging
string. Seen in young children. Disappears later. Heard in aortic area (I think)

Precordial inspection- don’t say anything unless there are positive findings
o Size, shape and type of chest
o Shape of precordium-
o Precordial bulge- good sign for detection in males is lateral
displacement of and elevation of left nipple. Causes of precordial
bulge
 Skeletal anomalies- scoliosis/kyphoscoliosis/rachitic
deformity
 Diseases of the lungs and pleura- bronchial
carcinoma/pleural effusion
 Diseases of the heart and pericardium- ventricular
hypertrophy/pericardial effusion
 Localised bulging could signify an aneurysm, possibly
secondary to MI
 o Backward bulges- pectus excavatum
o Apical impulse- - In the ____ ICS, ___ cm medial/lateral to the mid clavicular
line
o Check for the apical impulse tangentially
o Character should only be commented in palpation in the left lateral
position
o Causes of a non-localisable apical impulse- palpation
o Other pulsations in the precordium
o Visible parasternal heave- massive RV hypertrophy. Sometimes can
be due to LA enlargement.
o See-saw movements-
 In RV hypertrophy- inward movement of apex is associated
with outward movement of precordium during systole
 LV hypertrophy- reverse
o Pulsations in the high thoracic region (second right interspace)-
ascending aortic aneurysm/aortic regurgitation/dilation of aorta
o Pulsations involving the second or third left interspace- Pulmonary
artery dilation, hyperkinetic states, aneurysm of aorta
o Suprasternal pulsation- Can be physiological. Pathological causes are
due to aortic pathologies- AR, Aortic arch aneurysm
o Back pulsations- Coarctation of aorta (Suzman sign)
o Epigastric pulsation-
 Most commonly has two origins- abdominal aorta or right
ventricle
 From the right ventricle- coincides with the apex beat, and is
located higher up in the epigastrium
 From the abdominal aorta- physiologically in thin people,
due to AAA or due to a mass on the aorta. After apex beat
and located lower down in the epigastrium.

Apical impulse- In the ____ ICS, ___ cm medial/lateral to the mid clavicular line
o Definition***- Lowermost, outermost definite palpable cardiac impulse
o Check for the apical impulse tangentially
o The character of apical impulse must be commented on in the left lateral position.
o Apical impulse characters- (Dr. Hamide)
o RV apex- diffuse, not easily localisable, no special character
o LV apex- localised, can have a character
o Heaving- pressure overload
o Hyperdynamic- volume overload
o Tapping apical impulse- palpable first heart sound. It is not RV or LV type.
o Characteristics of a normal apical impulse
o Located in the left 5th ICS, ½ inch medial to the midclavicular line
o Confined to one ICS
o Has an area of around 2.5 cm2 (1.5 finger breadths)
 o Lasts for <1/3 of systole
o Causes of a non-locatable apical impulse- obesity, COPD, pleural effusion, behind the
rib. If you can’t locate it, search on the right side- for shifts/dextrocardia
o DR POPE- Non locatable apex- Dextrocardia, behind the Rib, Pleural effusion,
Obesity, Pericardial effusion, Emphysema (But never say dextrocardia first)
o Tapping apical impulse- In MS. It is palpable S1
o Heaving apical impulse-
o Normal location
o Confined to one ICS
o Increased duration and amplitude
o Duration is >2/3 of systole
o Due to pressure overload
o Causes- AS, Systemic hypertension, Coarctation of aorta
o Hyperdynamic apical impulse-
o Shifted downwards and outwards
o Occupies >1 ICS
o Normal duration but increased amplitude
o Due to volume overload
o Causes- MR, AR, High output states, VSD, PDA
o Retracting apical impulse- One which moves inwards in systole and outwards in
diastole. Causes: constrictive pericarditis, TR
 Hypokinetic Apical impulse- Myocardial infarction
 Double apical impulse-
o In HOCM- When the LV is ejecting blood, the mitral valve and the hypertrophied
interventricular septum nearly approximate, so there is a ‘second LV contraction’ to
overcome the obstruction
o Severe AS with AR
o LBBB
 Mechanism of apex beat- Isovolumetric contraction of the ventricle causes counterclockwise
rotation of the heart due to the spiral orientation of cardiac muscle fibres which causes the
apex to be palpable. The regression in amplitude is due to LV ejection.
Seesaw movement- The apex beat occurs in systole (when the LV contracts), however the
apex beat is a pulsation towards the chest wall. So, if the LV forms the apex, then if you put
one finger on the apex and one finger in the left parasternal area, the apex finger will go up
and the parasternal finger will go down in systole like a see-saw.
If the RV forms the apex, both will move together

A shifted apex is due to LV enlargement if it is shifted downwards and outwards (Volume

overload)
A shifted apex is due to RV enlargement if it is shifted only laterally

Parasternal heave
 o Parasternal area- the area from the 2nd-5th ICS enclosed from the midline to the
midpoint of the midline and the midclavicular line. Upper parasternal area is the 2 nd
and 3rd ICS. Lower parasternal area is the 4th and 5th ICS.
o Try and compress the heave and classify it as obliterable or non obliterable.
o Grading- AIIMS classification
o Grade III- Visible, palpable, non-obliterable
o Grade II- Visible, palpable, obliterable
o Grade I- Visible but not palpable
o Causes- RVH, LA enlargement

Facts about Mitral Stenosis

 Lutembacher syndrome- MS plus ASD
 Causes of haemoptysis in MS
o Rupture of pulmonary-bronchial venous connections (pulmonary apoplexy)
o Winter bronchitis or chronic bronchitis
o Acute pulmonary oedema
o Pulmonary infarction
o Warfarin overdose- rare
 Damped MS=Silent MS (for Dr.Hamide)
o In severe pulmonary hypertension, the right ventricle forms the apex, so the MDM is
no longer heard over the apex
 Juvenile MS
o Rheumatic in aetiology
o Age of onset <20 years
o Severe MS is common. Highly prone to get pulmonary HTN.
o Les prone for A. fib
o Immediate surgery should be done in symptomatic cases
 Complications of MS
o Atrial fibrillation
o Pulmonary hypertension, RV failure, Cor pulmonale
o Embolic stroke
o Acute limb ischaemia
o Mesenteric ischaemia
o Haemoptysis
o Very rare complications
 Ortner’s syndrome- LA enlargement causing RLN compression leading to
hoarseness, dysphagia due to oesophageal compression
 IE- very very rare (don’t say it). Also rare in ASD (I think)
 Significance of opening snap
o Indicates organic mitral stenosis
o Valve is pliable, no calcification
o S2-OS interval can be used to judge the severity of MS
o The MS is amenable to surgery
o Significant MS
o High LA pressure
 Clinical assessment of severity of MS
o S2-OS gap
  When MS is severe, LA pressure is very high, so the mitral valve is forced
open early after S2. Hence, the gap between S2 and OS is very less in severe
MS
o Duration of MDM- if OS occurs early, MDM will be longer signifying a more severe
MS
o Features of pulmonary hypertension
 Absent presystolic accentuation in MS
o Atrial fibrillation
o Left heart failure
o Massive LA thrombus
 Soft S1 in MS
o Co-existent MR
o Mitral valve calcification
o Digitalis overdose (prolonged PR interval)
o Acute rheumatic carditis (prolonged PR interval)
o A fib
o Damped MS- Pulmonary hypertension causing RVH which causes an RV apex

Typical findings in each of the valvular lesions

Aortic Stenosis

 Classified into
o Supravalvular
o Valvular
o Subvalvular
 Hypertrophic subaortic stenosis (HOCM)
 Fixed fibrotic subvalvular stenosis

Valvular aortic stenosis

Causes
 Rheumatic heart disease- Almost always associated with mitral valve involvement along with
aortic regurgitation.
 Congenital anomalies- bicuspid or unicuspid aortic valve
 Degenerative calcific stenosis

Classification- Normal valve area= 3-4 cm2

 Severe AS: <1 cm2
 Moderate AS: 1-1.5 cm2
 Mild AS: >1.5 cm2
Haemodynamics
 Left ventricular outflow tract obstruction (LVOT) occurs causing concentric left ventricular
hypertrophy (pressure overload)
 This can maintain normal haemodynamic function for years without decline in CO. However,
eventually the LV fails- systolic dysfunction
 The hypertrophied LV has a high oxygen demand- thus angina on exertion is common
Symptoms
 Usually asymptomatic until the stenosis becomes severe. Most presentations occur in the 6 th
to 8th decade. However, bicuspid aortic valve disease presents sooner.
 Exertional dyspnoea- due to increased pulmonary capillary pressure due to increased LVEDP
due to impaired relaxation of the poorly compliant hypertrophied LV.
 Angina pectoris- develops somewhat later due to increased oxygen demand.
 Exertional syncope- due to imbalance in vasoconstriction and vasodilation in exercising and
non exercising muscles
 In isolated severe AS, left heart failure and pulmonary hypertension occur very late.
Signs
 Usually sinus rhythm. AF suggests associated mitral valve disease.
 BP usually normal in the early stages. In the late stages, stroke volume declines so the pulse
pressure falls.
 Pulsus parvus et tardus- “rises slowly to a delayed peak”
 Carotid shudder- thrill palpable over the carotid arteries, especially over the left.
 Soft S2
o Calcification of the cusps
o Prolongation of left ventricular ejection time
 Accentuated a wave in JVP- Bernheim effect (diminished distensibility of the RV cavity due
to the bulging, hypertrophied interventricular septum)
 Laterally displaced apical impulse
 Systolic thrill
 Ejection click- audible especially in younger patients with bicuspid aortic valve. Inaudible
when the valve is calcified or rigid.
 Low pitched, rough and rasping ejection (mid) systolic murmur, best heard in the aortic area
in the sitting position with the breath held in expiration, radiating to the carotids.
 Gallavardin effect- transmission of AS murmur to the apex, where it is confused with MR.

Investigations
 ECG- LVH
 Doppler Echo
 Chest X Ray
 Cardiac catheterisation
Treatment
 Medical
o In severe AS, avoid strenuous physical activity
o ACE inhibitors and Beta blockers can be given to asymptomatic patients
o Serial Echo
 Surgical
o Indications
 Symptomatic severe AS
 LV systolic dysfunction
 Bicuspid aortic valve disease
 Aneurysmal root or ascending aorta
o Ross procedure- replacement of the aortic valve with autologous pulmonic valve and
implantation of a prosthetic pulmonic valve. Use has declined because of post op
complications and complexity of the procedure.
o Percutaneous Aortic balloon valvuloplasty
o Transcatheter Aortic valve replacement
Determinants of severity
 Single second heart sound- due to LV systole prolongation
 Pulsus parvus et tardus
 Louder and later peaking murmur

Supravalvular AS

 Usually caused due to a localised discrete narrowing above the sinuses of Valsalva.
 The area of highest intensity of the murmur is either the suprasternal notch or the first right
interspace. Radiation is more towards the right carotid as opposed to the left.
 a/w Hypercalcaemia, elfin facies- wide set eyes, upturned nose, small chin, patulous lips,
deep husky voice
 Stronger pulse and BP in the right arm and carotid as opposed to the left.
 Murmur is almost never associated with an ejection click.
HOCM
 Disproportionate and asymmetric thickening of the IV septum.
 As it bulges in systole, it draws the anterior mitral leaflet medially, thus causing LVOT
obstruction.
 Because this degree of obstruction depends on the proximity of the anterior mitral leaflet
and the IV septum, the murmur characteristically increases with manoeuvres which
decrease the left ventricular size like inspiration, tachycardia, amylnitrite, standing after
squatting
 Can have a bifid pulse
 Can have double or triple apical impulse

Aortic Regurgitation

Causes
 Valvular causes
o Congenital- bicuspid aortic valve
o Rheumatic heart disease
o Endocarditis
o Myxomatous (prolapse)
o Syphilis (Luetic Aortitis)
o Ankylosing spondylitis
o Trauma
 Root disease
o Aortic dissection
o Cystic medial degeneration
o Marfan’s
o Bicuspid aortic valve
 Aortitis

Haemodynamics
  Total stroke volume increases
 Increase in LVEDV occurs (increased preload).
 Volume overload results in dilation and eccentric hypertrophy
 Ultimately, the LV fails
 In acute severe AR, as in endocarditis, the LV cannot compensate rapidly so pulmonary
oedema occurs.
 In chronic severe AR, the patients can be asymptomatic for up to 10-15 years.

Symptoms
 Palpitations can be an early complaint- can be seen for years before the exertional dyspnoea
 Angina can occur
 Then exertional dyspnoea, PND, orthopnoea

***Signs

 Peripheral signs (from head to toe)

o Lighthouse sign- alternate flushing and blanching of forehead
o Becker’s sign- retinal artery pulsations
o Landolfi sign- changes in pupil size with cardiac systole
o Muller’s sign- uvula pulsation
o De Musset’s sign- head bobbing
o Corrigan’s sign- dancing cartotids
o Locomotor brachii- tortuous and highly pulsatile brachial artery
o Hill’s sign- Lower limb systolic BP more than 20mm Hg above UL SBP (Note: LL BP
can be measured in the popliteal artery with a lower limb cuff over the thigh, or over
the posterior tibial artery with the cuff tied just above the medial malleolus)
 >20 mm Hg- mild AR
 >40 mm Hg- moderate AR
 >60 mm Hg- severe AR
 Cause: It is an artefact of the sphygmomanometer (ie intra arterial
measurements are the same in the UL and LL arteries). It is believed that the
reflected waves from the periphery summate with the forward waves of the
central arteries (ref- Jules Constant)
 Falsely low Hill’s sign (ie the difference in BP is lower than the actual severity
of AR)
 CHF- due to decreased stroke volume. Presence of Hill’s sign
depends on myocardial contraction.
 Severe AS
o Corrigan’s pulse- Water hammer/collapsing pulse
o Quincke’s sign- alternate flushing and pallor when light pressure is applied to the
nail bed
 o Suprasternal pulsations
o Rosenbach sign- Pulsations in liver
o Gerhardt’s sign- Pulsations in enlarged spleen
o Durozeiz murmur- Diastolic murmur on compression of the femoral artery distally
o Traube’s pistol shot femorals- Booming sound produced after pressing the
stethoscope over the femoral artery
o Systolic murmur on compression of the femoral artery proximally
 Heaving apical impulse???? Displaced down and out
 Pulsus bisferiens
 Diastolic thrill over aortic area
 Systolic thrill may be felt over the carotids and suprasternal notch and need not mean there
is an accompanying AS.
 In severe AR, A2 is usually absent.
 High pitched, blowing, decrescendo, diastolic murmur, best heard in the 3 rd ICS along the left
sternal border in the sitting position with breath held in expiration
 When the murmur is best heard over the right sternal border, it suggests that the
regurgitation is due to aneurysmal dilation.
 A mid systolic ejection murmur can also be heard best in the aortic area and transmitted to
the carotids
 Austin Flint murmur- soft, low pitched, rumbling mid to late diastolic murmur mimicking
that of MS. The AR stream may impinge on the undersurface of the anterior leaflet of the
mitral valve and push it up, creating a relative MS.
 Cole Cecil murmur- AR murmur best heard over apex or even axilla or mid left thorax

Investigations
 ECG- LVH
 Doppler Echo
 CXR
 Cardiac cath
Management

Murmur is characteristically an early diastolic murmur best heard over Erb’s point (neo
Aortic area) because of the orientation of the aorta. However, if the AR murmur is better
heard in the Aortic area, it suggests an aortic aneurysm causing AR.

Dissection causes AR due to displacement of the valves

Mitral Stenosis
 Causes
 Rheumatic heart disease
 Congenital mitral stenosis
 Severe mitral annular calcification
 SLE, Rheumatoid Arthritis
 Hunter’s syndrome, Hurler’s syndrome

Congenital MS
 Supravalvular- fibrous ring
 Valvular-
o Fusion of commissure and papillary muscle
o Excessive valvular tissue
o Annular hypoplasia
 Subvalvular
o Single papillary muscle- parachute valve
o Abnormally large or numerous papillary muscle- Hammock valve
o Absent papillary muscle

Classification- Normal mitral valve area is 4-6 cm2

 Mitral valve area <1cm2- very severe MS/tight MS/critical MS

 Mitral valve area 1-1.5cm2—severe MS
 Mitral valve area >1.5 cm2- progressive MS

Haemodynamics
 A gradual rise in LA pressure tends to cause an increase in pulmonary vascular resistance
which leads to pulmonary hypertension that protects vs. pulmonary oedema
 A sudden rise in LA pressure, like in A fib (d/t decreased atrial contraction) causes pulmonary
oedema
 Up to severe MS, the elevated LA pressure is enough to maintain cardiac output, so CO and
Ejection fraction will be normal. However, with conditions that increase the heart rate, the
atrial kick is not possible so the CO decreases.
 In patients whose mitral orifices are large enough to accommodate a normal blood flow with
only mild LA pressure elevation, marked LA pressure elevation leading to dyspnoea and
cough can be precipitated by sudden changes in HR, volume status or CO like fever,
excitement, severe exertion, severe anaemia, paroxysmal AF, pregnancy, thyrotoxicosis
 Causes of PAH-
o Passive backward transmission of the elevated LA pressure
o Pulmonary arteriolar constriction (second stenosis)- due to LA and pulmonary
venous hypertension (reactive pulmonary hypertension). These two are the main
mechanisms.

Symptoms

 The latent period between the attack of rheumatic carditis and development of symptoms
due to MS is about two decades.
 Dyspnoea- pulmonary congestion stimulates the J receptors in the interstitum. The initial
bouts of dyspnoea are due to elevated pulmonary vascular pressures which decrease the
pulmonary compliance causing dyspnoea on exertion.
 Fatigue- decreased cardiac output
 Oedema, ascites- RHF
 Palpitations- A fib because of stretching of pulmonary veins
 Haemoptysis- due to rupture of pulmonary-bronchial venous connections secondary to
PAH
 Cough- pulmonary congestion
 Chest pain- PAH
 Stroke, limb ischaemia- emboli
 Recurrent pulmonary emboli can occur
 Pulmonary infections- bronchitis, bronchopneumonia, lobar pneumonia complicate
untreated MS, especially in winter months.

Signs
 A fib
 Mitral facies- malar flush with pinched and blue facies
 JVP may have prominent a waves due to pulmonary hypertension
 Loud S1, opening snap, MDM
 Crepts, pulmonary oedema, effusions
 Parasternal heave, Loud P2.

Investigations
 ECG- A fib / bifid P waves (P mitrale) associated with LA hypertrophy/ RV hypertrophy- tall R
waves in V1, V2
 CXR-
o Left atrial enlargement- double shadow behind the heart in right heart border-
shadow within a shadow
o Straightening of left heart border due to prominent pulmonary artery and LA
appendage
o Kerley B lines- dense, short, horizontal lines most commonly seen in costophrenic
angle when pulmonary venous pressure is between 20-30 mmHg
 o Kerley A lines- straight, dense lines running towards hilum when pulmonary venous
pressure is more than 30 mmHg
 Doppler Echo- thickened immobile cusps, reduced valve area, enlarged LA, reduced rate of
diastolic filling of LV
o Abascal or Wilkins Echocardiography score
 Leaflet mobility
 Valve thickness
 Subvalvular thickening
 Valvular calcification
o Wilkins score of <8/16 means the valve is amenable to BMV. Otherwise, surgery is
advised
 Cardiac cath- Check for coronary artery disease, pulmonary artery pressure, MS, MR

Management options
 Closed mitral valvulotomy/commissurotomy- Preferred in patients with pliable valve
without associated MR. Done with the aid of TUBBS transventricular dilator
 Balloon mitral valvuloplasty
o Criteria
 Significant symptoms
 Isolated MS
 No MR
 Mobile non calcified valve
 No LA thrombus
o Complications
 Embolic events
 Cardiac perforation
 MR
 Iatrogenic ASD
 Valve replacement
o When associated MR is present or valve is rigid and calcified
o Mechanical prostheses
 Caged ball valve- Starr-Edwards prosthesis
 Tilting disc valve- St. Jude, Bjork-Shiley valves
 Tilting-disc preferred to caged ball because
 It occupies less space
 Less incidence of haemolysis
 Less incidence of strut fractures
o Bioprosthesis
 Porcine
 Pericardial xenograft
 Cadaveric valve
 Lower incidence of thromboembolism
 Not useful in patients <65 years of age due to rapid deterioration
 ***Causes of Mid diastolic murmur at apex
 Mitral stenosis
 Left Atrial Myxoma
 Austin Flint Murmur (MDM in AR)
 Carey-Coombs murmur (MDM in Acute Rheumatic Fever)
 Ball valve thrombus in the left atrium
 Increased flow across non stenotic mitral valve- MR, VSD, PDA, high output states, complete
heart block

Causes of MDM at other areas

 Tricuspid stenosis
 Increased flow across non stenotic tricuspid valve- ASD, TR, TAPVR
 Right Atrial Myxoma

Differential Diagnoses

1. Atrial Septal Defect: Evidence of RV enlargement and PAH is often seen in both. Fixed split
of S2 and mid systolic murmur at left sternal border go in favour of ASD. ASDs with large left
to right shunts can result in functional TS because of enhanced diastolic flow.
2. Left Atrial Myxoma: Can cause dyspnoea and a diastolic murmur. However, the patients
have features suggestive of systemic disease like weight loss, fever, anaemia, systemic
emboli, elevated IgG and IL-6. The auscultatory findings change markedly with body position.
3. Significant MR: Can be associated with a prominent diastolic murmur at the apex due to
increased anterograde flow. But, OS and Loud P2 are absent and S1 is soft or absent.
Obviously, a loud PSM will be heard.

Severe AR: Austin Flint murmur can be mistaken. It is not intensified in presystole and becomes
softer with the administration of vasodilators

Management
 Medical- Penicillin V 250 mg BD
  If Rheumatic fever, 250 mg QID
 If established heart disease, lifelong
 Atrial fibrillation- Digoxin 0.25mg 5 days a week OD
o Digoxin toxicity
 If rate not controlled by Digoxin, Diltiazem/Atenolol can be given orally
 Warfarin
 Diuretics
 Emergency AF- rapid digitalisation 0.25 mg IV bolus, wait for 2 hours. If no
improvement, 0.25 mg again until max 1 mg. if it does not work, beta blockers
Surgical-MVR
Newer techniques in MVR
Other points about MS

 Most common location of the thrombus is in the left atrial appendage (left auricle)
 The time interval between A2 and the opening snap correlates with the severity of MS. Even
the duration of the murmur can correlate.
 Silent MS- When the CO is markedly reduced in MS, the typical auscultatory findings may
not be detectable.
 Note: The quality of S1 is dependent on dP/dT of the left ventricle. So any conditions altering
this will alter the quality of S1

 Other causes of Loud S1:

o Hyperdynamic circulatory states
o Holosystolic MVP with MR- the prolapse delays the tension of the leaflet, thus
allowing it to close at the peak of ventricular contraction
o LA myxoma- the tumour delays the closure of the valve
o Short PR interval
 P represents atrial contraction, and R represents ventricular contraction.
 If the PR interval is short, the ventricular contraction occurs so quickly after
the atrium has contracted that the LA has not had enough time to relax
(short x descent).
 Therefore, atrial pressure is still at a high level when pressure in the LV
exceeds it enough to close the mitral valve. The LV pressure has to reach a
higher level, which corresponds to a higher slope on the dP/dT curve which
causes a loud S1
o WPW, Ganong levine syndromes- same mechanism
o Ebstein anomaly
 Loud S1 in MS (Ref- Braunwald’s/10e p. 1473)
o Because of increased LA pressure, the LV pressure has to rise to a higher value to
force the valves shut. This occurs at a higher pressure gradient on the LV Pressure-
volume curve which causes a louder sound (dP/dt theory)
o Because the high A-V pressure gradient at the onset of systole keeps the valves
maximally separated, there is an increased closing excursion of the leaflets
 Causes of Soft S1
o Calcific mitral stenosis
o Aortic regurgitation- In sudden severe AR, the mitral valve may be closed in mid-
diastole and is associated with a soft or inaudible S1
o Prolonged PR interval (heart block) due to late closure of mitral valve
o MI, CHF, LBBB

Mitral Regurgitation

Causes
 Acute MR: Endocarditis, Post MI papillary muscle rupture (posteromedial), Chordal
rupture/leaflet fall due to MVP and IE, Trauma
 Chronic MR: MVP, Rheumatic Fever, healed endocarditis , mitral annular calcification,
congenital cleft, HOCM with SAM, Dilated cardiomyopathy

Haemodynamics

 Chronic MR causes gradual dilation of the LA with little increase in pressures and therefore
causes very few symptoms. Still, the LV dilates slowly and the LA and LV pressures gradually
increase due to chronic volume overload.
 Increased LV volume is often accompanied by a reduced cardiac output (verify this)
 Acute MR causes a rapid rise in LA pressure because of normal LA compliance and marked
symptomatic deterioration

Symptoms
 Dyspnoea
 Fatigue- decreased cardiac output
 Palpitations- A fib, increased stroke volume
 Right heart failure in late stages

Signs
 A fib
 Cardiomegaly with a displaced hyperdynamic apex
 Apical PSM ± thrill
 Soft S1, S3
 Signs of pulmonary venous congestion- crepts, oedema, effusions
 Signs of pulmonary hypertension and right heart failure.

Investigations
 ECG- Left atrial hypertrophy, Left ventricular hypertrophy/ A fib
 CXR-
o Inverted moustache
 o Enlarged LA, LV, Pulm venous congestion, Pulm oedema if acute
 Echo- Dilated LA, LV
 Doppler
 Cardiac cath
Causes of systolic murmurs
 Pansystolic murmurs- MR, TR, VSD
 Early systolic murmur- Acute MR, Muscular VSD, Acute TR
 Mid systolic murmur- Supravalvular aortic stenosis, Coarctation of aorta, Aortic stenosis,
Aortic sclerosis, HOCM, Increased flow, Pulmonic stenosis, Supravalvular Pulmonic Stenosis,
ASD (flow murmur)
 Late systolic murmur- MVP, Acute MI, TVP

ASD
 Types
o Ostium secundum ASD- 90%
o Ostium primum ASD 5%- commonly associated with Down syndrome or endocardial
cushion defects
 Syndromic associations
o Holt-Oram syndrome
 Triphalangeal (fingerised) thumb, sometimes abrachia or phocomelia
o Patau syndrome
 Trisomy 13
 Polydactyly, flexion deformity of fingers, simian crease, cleft lip and palate,
microcephaly
 ASD, VSD, PDA
o Edward syndrome
 Trisomy 18
 Prominent occiput, low set malformed ears, rocker bottom feet,
micrognathia, clenched fists
 ASD, VSD, PDA
o Ellis van Creveld syndrome (polydactyly, nail dysplasia, dwarfism)
 Atrial fibrillation is common in ASD
 Symptoms and signs
o Small defects are usually asymptomatic
o Large defects present with features like tachycardia, right heart failure, left heart
failure, exertional dyspnoea
 Signs
o Associated PS can be present
o Wide fixed split of S2
o S2 split is narrowed with the development of pulmonary hypertension
o Flow ESM across pulmonary valve
o Flow MDM across mitral valve
 DDs
o MS with pulmonary HTN
o Partial anomalous pulmonary venous connections
o Total anomalous pulmonary venous connections with a large interatrial
communication without pulmonary HTN
TR vs. MR

TR has:
 Murmur best heard in tricuspid area
 Positive Carvallo’s
 Hepatic pulsation
 Response to abdominojugular reflux- Vitum sign
 Giant V waves with deep Y descents- Lancisi sign
 Earlobe pulsation

Acute MR causes an early systolic murmur. This is because a dilated LA needs to be present
for a PSM to occur and in early MR the LA is not capable of dilation, so the LV and LA
pressure equalises in early systole itself.

TOF

Character Aortic Stenosis Pulmonic Stenosis

Murmur best heard at Right 2nd ICS Left sternal border
Effect of inspiration Murmur intensity decreases Increases
Standing Makes the PS murmur
louder in inspiraton
Ejection click May be present May be present, but
disappears in inspiration

VSD
 Muscular VSD- crescendo decrescendo murmur because ventricular contraction
closes the hole towards the end of systole
 Membranous VSD- PSM

Cardiac cycle

Rheumatic Fever
 Acute Rheumatic Fever is most commonly a disease of children aged 5-14. They are
rare in people >30 years. RHD however peaks between 25-40 years.
 Cause- Group A Streptococci
 Pathogenesis- molecular mimicry: immune response targeted at streptococcal
antigens (M protein and NAG) also recognises human tissues.

Statistics

 Mitral stenosis is seen in 99% of RHD cases

 40% of cases have MS with MR. Isolated MS is seen in 25% of cases.
 38% of cases have multivalve involvement. 35% have aortic valve involvement, 6%
have Tricuspid valve involvement. Pulmonary valve is very rarely involved.

Clinical features
 Latent period of 1-5 weeks. The preceding infection is commonly subclinical but can
be confirmed by antibody testing.
 m/c c/f- polyarthritis (60-75%), carditis (50-60%)

Heart involvement
 Up to 60% of patients of ARF progress to RHD.
Endocardium/myocardium/pericardium may be involved.
 Mitral valve is almost always affected, sometimes together with the aortic valve.
Isolated aortic valve involvement is rare.

 Early valvular damage leads to regurgitation. Over ensuing years, usually as a result
of recurrent episodes, leaflet thickening, scarring, calcification and eventually
valvular stenosis may develop.
 The characteristic manifestation of carditis in previously unaffected individuals is
MR, sometimes accompanied by AR.
 Myocarditis- may lead to first degree AV block and softening of S1.
Joint involvement
 Hot, swollen, red, tender joints and polyarthritis
 Typically migrates over a period of hours.
 Commonly affects the large joints, and is asymmetric. Pain is usually severe and
disabling until anti-inflammatory therapy is commenced. It is characteristically
sensitive to NSAIDs/Salicylates
Chorea
 Syndenham’s chorea commonly occurs in the absence of other manifestations, has a
prolonged latent period, and is more common in females.
 Chorea is always associated with carditis
 Especially affects the head causing characteristic darting movements of the tongue,
and upper limbs.
 May be generalised or restricted to one side of the body
 Often associated emotional lability or obsessive-compulsive traits
 Chorea itself usually resolves around 6 weeks, but may take up to 6 months.
Skin
 Classic rash- erythema marginatum- begins as pink macules that clear centrally,
leaving a serpiginous spreading edge.
 The rash is evanescent, appearing and disappearing before the examiner’s eyes
 Usually occurs on the trunk, sometimes on the limbs, but almost never on the face
 Subcutanous nodules- 3 P’s- painless, pea sized, on bony prominences. Last for a few
days to few weeks.
 Investigations
 ESR, CRP
 WBC count
 Blood culture if febrile
 Throat swab before giving antibiotics
 ECG
 Chest X ray

Treatment

 Antibiotics- Phenoxymethylpenicillin 500mg PO bd/Amox 50 mg/kg daily for 10 days.

 Salicylates and NSAIDs: Used to treat arthritis/arthralgia/fever, once the dx is
confirmed. Of no value in treatment of carditis and chorea. Aspirin 50-60 mg/kg/day
up to 80-100 mg/kg/day in 4-5 divided doses. Monitor for salicylate toxicity.
Naproxen 10-20 mg/kg/day in two divided doses is an alternative.
 Severe carditis can be treated with steroids, but it is controversial. The benefits must
be balanced against the risks. Prednisolone 1-2 mg/kg/day for a few days, maximum
of 3 weeks
 Severe chorea can be controlled with Carbamazepine. Response may not be seen for
1-2 weeks and the medication should be continued for 1-2 weeks after the
symptoms subside. Steroids can be considered in very severe or refractory cases.
Prednisolone 0.5 mg/kg/day with rapid weaning. IVIg is not recommended except in
severe chorea refractory to other treatments.

Prevention

Primary prevention

 Timely and complete treatment of group A streptococcal sore throat with antibiotics
 If commenced within 9 days of sore throat onset, a complete course of penicillin will prevent
almost all cases of ARF from developing.

Secondary prevention
 Benzathine penicillin G 1.2 million units every 4 weeks.
 RF without carditis- for 5 years after the last attack or until 21 years of age (whichever is
longer)
 RF with carditis but no residual valvular disease- For 10 years after the last attack or until
21 years of age, whichever is longer.
 RF with persistent valvular disease, clinically or subclinically evident- 20 years after the
last attack or until 40 years of age, whichever is longer.

Facies in congenital heart disease- Nice to know