CARDIOVASCULAR SYSTEM

Case Sheet Performa

Name:

Age:

Sex:

Address:

Occupation:

Religion:

Chief complaints:

History of present illness:

Past history:

Family history:

Personal history:

Treatment history:

General physical examination

Pallor

Ictherus

Cyanosis

Klubbing

Lymphedenopathy

Edema:

Vitals
Respiratort rate
Pulse rate

Temperature

blood pressure

Systemic examination
Cardio vascular system.

Inspection:-
1. Shape of chest precordium
2. Position of apical impulse
3. Position of trachea
4. Visible pulsations
5. Any dilated veins
6. Any other findings:

Palpation:
1. Apex beat
2. Parasternal heave/impulse
3. Palpable pulsations
4. Palpable sounds/thrills
5. Any other findings:
Tenderness??

Percussion:
1. Cardiac dullness

Auscultation:
1. Heart sounds
a. Mitral area
b. Tricuspid area
c. Aortic area
d. Pulmonary area
2. Splitting of heart sounds
3. Additional sounds(clicks,opening snap and rub)
4. Murmurs
 Cardiovascular system
Cardinal symptoms:

1. Dyspnoea
 Onset
 Duration
 Progress
 Grade
 Aggrevating/Relieving factors –respiratory, posture, medications
 Orthopeo/PND

Onset:
Sudden Gradual
Acute left heart failure Cardiomyopathy
Myocardial infraction Left sided valvularheart disease
Mitral stenosis Hypertensive heart disease

Grading of dyspnoea( new York heart association)

Grade I – patients with cardiac disease but no dyspnoea on oedema physical activity

Grade II – comfortable at rest but dyspnoeic on ordinary physical activity

Grade III – marked limitations of physical activity dyspnoic on less than ordinary physical
activity

Grade IV – dyspnoea at rest and increases with mildest coccertion.

Orthopnoea –

 Dyspnoea in recumbent position (lying flat) which is relieved by sitting up or elevation

of head with pillows.
 Ex:-Acute left heart failure
Acute congestion cardiac failure

Paraxysmal nocturnal dyspnoea:

 Attacks of breathlessness occuring at night and awaken the patient from sleep
 Ischemic heart disease
 Aortic valve disease
  Left heart failure
 Cardionyopathy

2. Chest pain:

a) Site
b) Duration
c) Onset
d) Type
e) Radiation
f) Severity
g) Aggrevating/Relieving factors

Site:
1) Retrosternal central –
a. Angina Pectoris
b. MI
2) Precordial area – pericarditis pain
3) Anterior chest – aortic dissection pain

Duration:
 Short – angina pectoris
 Long –
o MI
o Pericardites
o Aortic dissecting aneurysm

Onset:
 Sudden –
o Angina pectoris
o Aortic dissecting aneurysm
 Gradual –
o Myocardial infraction
o Pericarditis
Type:
1. Tightness/pressing/squeezing/heaviness:
a. Angina pectoris
b. Myocardial infraction
2. Tearing/ripping –
a. aortic dissection aneurysm
3. Sharp cutting/ stabbing :
a. Pericarditis.

Radiation:
1) To arms (left)neck ,Shoulder, lower jaw –
a. Angina pectoris
b. MI
2) Tip of shoulder back – pericarditis
3) Anterior chest radiating to neck, back, abdomen – Aortic dissecting aneurysm

Aggrevating /Relieving factors:

1) Angina pectoris
Aggrevating factors:-
a. Excertion
b. Cold
c. Heavy meds
d. Stress

Relieving factors:-

a. Rest
b. NTG(nitroglycerin)
2) Pericarditis:
Aggrevating factors:-
a. Breathing
b. Coughing
c. change in posture
Relieving factors:-
a. forward bending gives relief
3) Aortic dissecting aneurysm:-
Aggrevating factor:- hypertension
Relieving factor:- absent
 Ischemic cardiac pain Non cardiac pain
Location Central, diffuse Peripheral localized
Radiation Neck/shoulder/arm/jaw/back No radiation
Character Tight squeezing Sharp stabbing
Aggrevating factor Exertion, stress Postur,breathing
Relieving Factor Rest,nitrate Absent
Associated symptoms Breathlessness Respiration, GIT, locomotor
symptoms

3. Palpitations:-
 Onset
 Duration
 Timing
 Aggrevating/Relieving factors
 Associated symptoms

Onset, duration:
Sudden and short Gradual and long
Atrial fibrillation Sinus tachycardia
Atrial flutter Anxiety states
Paroxysmal supra ventricular tachycardia
(PSVT)

Timing:
Regular:

causes

o Exertion
o Caffeine
o Hyperthyroidism

Irregular:
 causes

o Ventricular ectopics
o Atrial fibrillation
o Ventricular tachycardia
o Atrial tachycardia

Aggrevating factors:
o Anemia
o Coffeine
o Thyrotoxicosis
o Pheachromocytoma
o Pyrexia

Relieving factors:
o Vomiting
o Rest

Associated symptoms:
1. Palpitation + polyuria – Supraventricular Tachycardia
2. Palpitation + breathlessness – Atrial Fibrillation, Ventricular Tachycardia

4) Syncope-

a. Onset- mostly sudden

b. Duration
c. Timing of day
d. Premonitory symptoms (warning signs)
i. Nausea
ii. Blurring of vision
iii. Noises in ears
iv. Vertigo
v. Feeling of warmth
vi. Dry mouth
vii. Deep sighing respiration
viii. Sweating
 ix. Desire for fresh air/water

Causes:
 Heart block
 Ventricular tachycardia
 Extreme bradycardia
 Aortic stenosis
 Hypertrophic obstruction cardiomyopathy
 Left atrial tumours
 Drugs : ACE inhibition, nitrates, beta blockers

5) Oedema:

 Onset- usually gradual

 Distribution – first legs/ankle
 Periodicity- most severe during evening time
 Aggrevating factor- long standing
 Relieving factors- rest with leg elevation
 Type- cardiac conditions have pitting type of oedema.
 Cardiac causes of oedema:
 Congestive heart failure
 Constrictive pericarditis.
 Pericardial effusion

6) Fatigue:
 Duration
 Frequency
 Timing of day
 Aggrevating factors- physical activity
 Relieving factors- rest
 Causes:-
 Heart failure
 Cyanotic heart disease
  Coronary heart disease

Past history:
 H/o similar illness
 H/o hypertension,diabetes mellitus
 H/o Ischaemic heart disease, Coronaryheart disease, myocardial infraction
 H/o congenital heart problems
 Any surgery/Angiogram
 H/o maternal rubella infection – Congenital heart disease in the foetus
 Migrating joint pain – rheumatic heart disease

Family history:
 Any similar condition in relatives
 Hypertension,diabetes mellitus,coronary heart disease,hyperlipidemia
 Consanguinous marriage

Personal history:
Appetite- normal/increased/decreased

Diet – veg/ no veg

Bowel-normal/constipation/loose/irregular

Bladder-normal/frequency/burning sensation/dribbling

Habit addiction – smoking/alcohol

Sleep-sound/disturbed

Treatment history:
 Any allergies
 Any H/O hospitalization
 Any present medications
 General examination

 Eyes:
o Pallor:anaemia
o Ictherus: jaundice
o Xanthelasmaa: hyperlipidemia
o Roths spots : Infective endocarditis
o Lens:
o Up: marfans syndrome(aortic dissection)
o Down: homocystinuria

 Nails:
o Clubbing-cyanotic heart disease like tetralogy of fallot ,subacute bacterial
endocarditis
o Splinter haemorrhage – Subacutebacterial endocarditis,infective endocarditis.
o Cyanosis-tetralogy of fallot,heart failure,myocardial infraction.
o Pale – anaemia
o Red half moons (red lunula)-congestive heart failure

 Skin:
o Bluish tinge – cyanosis
o Pallor – anaemia

 Face:
o Malar flush over cheeks-mitral stenosis
o Low set ears-downs syndrome(atrioventrivular septal defect,mitral valve
defects,tetralogy of fallot
o Erythemia margenation-rheumatic fever
o Sub cutaneous nodules-rheumatic fever

 Neck:
o Lymphodenapathy-
 o Webbed neck-turners syndrome(aortic stenosis,coarctation of aorta)

 Skeletal deformity
o Pectus carinatum-turners syndrome(aortic stenosis,coarctation of aorta)
o Pectus excavatum- marfans syndrome(aortic dissection)
o Shield chest- turners syndrome(aortic stenosis,coarctation of aorta)
o Cubitus valgus- turners syndrome(aortic stenosis,coarctation of aorta)

 Extremeties:
o Oslers nodes-infective endocarditis
o Palmor erythema (janeway lesions)-infective endocarditis
o Cold extremeties-heart failure
o Syndactyly, polydactyly, arachnodactyly-down syndrome,marfan syndrome
o Ankle oedema-congestive heart failure

VITALS

Temperature – Infective endocarditis, Congestive heart failure, rheumatic fever

Respiratory Rate:

Blood pressure:
 Recorded with sphygmomanometer
 Method:
Measured by palpatory and auscultatory mothod
1. Arm supported at the heart level
2. All clothing from arm removed
3. Apply the cuff to the arm and palpate the brachial pulse
4. Inflate the cuff until the pulse is impalpable. The pressure at which the pulse is
impalpable gives a rough estimation of systolic pressure. This is the palpatory
method.
 5. Now inflate another 20-30 mm Hg above the pressure at which the pulse was
impalpable and auscultate over the brachial artery through the stethoscope
6. Deflate the cuff slowly until the korotskoff sounds (regular heart sounds)can be
heard.
7. The pressure at which the korotskoff sounds become audible indicates the systolic
pressure.
8. Continue to deflate the cuff slowly until the sounds disappear. The pressure at
which the korotkoff sounds disappear indicate the diastolic pressure.

Korotkoff sounds: As the sphygmomanometer is deflated the korotkoff sound get louder
then become muffled and disappear in the following phases:

 Phase I – appearance of korotkoff sounds as clear tapping sounds marks systolic blood
pressure
 Phase II – tapping sounds become murmur in nature
 Phase III – murmurs become louder
 Phase IV – sounds become muffled in nature
 Phase V – disappearance of sounds marks diastolic blood pressure

Note:
1. Ask the patient to relax for 5 minutes before measuring for accurate reading
2. Advice the patient to avoid smoking, coffee 30 minutes before measuring blood pressure
3. The arm must be supported at heart level.
4. Clothing on arm removed. The cuff should cover 2/3 of distance between the patients
elbow and shoulder or the length and width of the bladder inside the cuff should be 80%
and 40% respectively of upper arm circumference.
5. The cuff should be positioned or placed above the antecubital fold such that the lower
edge of the cuff should be one inch or 2-3cm above antecubital fold.
6. The midportion of the bladder within cuff should be over the brachial artery.
7. Place the chest piece of the stethoscope in the antecubitall space below the cuff.
8. The deflation should be at a rate of 2-3 mm Hg per second.

Mistakes Increase Decrease

Small cuff 10-40 mm Hg No decrease
Cuff over clothing 10-40 mm Hg 10-40mmHg
Legs crossed 5-8 mmHg No decrease
Talking patient 10-15mmHg No decrease
No rest before recording bp 10-20mmHg No decrease
Full bladder 10-15mmHg No decrease
Pain 10-30mmHg No decrease
Arm below heart level 1.8mm Hg/inch No decrease
Arm above heart level No increase 1.0 mm Hg/inch
Normal:
JNC 8 classification of HTN

Category Systolic mm Hg Diastolic mm Hg

Normal < 120 < 80
Prehypertension 120-139 80-89
Hypertension
First stage 140-159 90-99
Second stage >160 >100

 Note: In aortic regurgitation the diastolic blood pressure might be 0 mm Hg or even heard
after deflating the cuff.
 In obstruction lesions of aorta, innominate or subclavian arteries the differences in
systolic pressure between both the arms may exceed 10 mm Hg
 Normal systolic pressure difference between both upper arms is 5 mm Hg.
 Systolic pressure difference between upper and lower extremities is 10 -15 mm Hg but
diastolic is same.
 In coartation of aorta the systolic pressure difference between upper and lower
extremities exceeds 20 mm Hg.

Postural /orthostatic hypotension:

 A fall in systolic pressure more than >20 mm Hg when patient stands from lying posture
is postural/orthostatic hypotension.

Pulse rate:
A pulse rate is a pressure wave moving rapidly through the arterial system felt by the
finger produced by cardiac systole.

Various pulses:

1. The brachial pulse

2. The carotid pulse
3. The femoral pulse
4. The dorsalis pedis pulse
5. The poplitial pulse
6. The posterior tibial
Method: palpate the pulse with three fingers for one full minute.

1. Radial pulse: Patient may sit or lie down. The elbow is slightly flexed and forearm mid
pronated. Palpate on the lateral aspect of forearm just below the base of thumb.
2. Brachial pulse: palpate towards the by medial side in the antecubital fossa . compressing
against the humerus with your index , middle fingers or thumb of the opposite hand.use
your free hand, to flex elbow till the pulsation are felt.
3. Carotid pulse: Ask the patient to lie down, palpate in the neck by compressing against the
transverse process of cervical vertebrae with left thumb for right carotid and right thumb
for left carotid.
4. Femoral pulse: Ask the patient to lie down, palpate in the upper inner thigh at mid
ingunal point, midway between the pubic symphysis and anterior superior iliac spine.
5. Dorsalis pedis pulse: palpate on the dossum of the foot just lateral to the extensos hallucis
longus tendon of great toe.
6. Poplitial pulse: it lies in the popliteal fossa at the back of the leg. Place your hands around
the knee with knee flexed about 45 degree, push your finger tips into the popliteal fossa
with the thumbs lying on the patient patella.
7. The posterior tibial: palpate behind and slightly below the medial malleolus of the ankle
that is midway between posterior border of medial malleolus and achillis tendon.

Arterial pulse is assessed for the following:

1. Rate
2. Rhythm
3. Volume
4. Character
5. Delays-radioradial,radiofemoral
6. Arterial wall

1. Rate:
 Radial pulse is most commonly used as it is superficial.
 If pulse is regularly count for 30 sec and multiply by 2.
 If pulse is irregular count for one minute and also calculate pulse deficit.
Pulse deficit = HR(heart rate) –PR(pulse rate)
HR is counted with the help of stethoscope
Mostly PD > 10 beats/min = atrial fibrillation
PD < 10 beats/min = ventricular ectopics

Normal : 60 – 100 bpm

 Bradycardia - <60/min
(Sinus bradycardia)
Causes:
o Sleep
o Athletes
o Hypothyroidism
o Hypothermia
o Raised ICT
o Heart block
o Obstructive jaundice
o Drugs:beta blockers, Calcium channel blockers, digoxin

Tachycardia: > 100/min

(Sinus tachycardia)

Causes:

o Exercise
o pain
o Anxiety
o Thyrotoxicosis
o Hypovolemia
o Congestive heart failure
o Pheochromcytoma
o Drugs: beta agonists salbutamol, atropine, nifedipine

Rhythm: Sinus rhythm is regular

Irregular rhythms:

a) Regularly irregular rhythm:

a. Pulse rate is irregular but in a repetitive but in a repetitive pattern.
Ex: 1. Ventricular ectopics in bigemini, trigemini

2. atrial flutter with fixed Av conduction

b) Irregularly irregular rhythm:

Pulse rate is completely irregular and unpredictable
I. Atrial or ventricular ectopics
 II. Atrial fibrillation

Volume:
Depends on the pulse pressure

Method:

 Pulse volume depends on the amplitude by which the finger is lifted while palpating the
pulse.
 No lift of fingers – normal volume
 Lifting of finger present – high/good volume
 No lifting and pulse felt with difficulty = low volume
Good or high volume = >60 mm Hg pulse pressure
Normal volume = 30 – 60 mm Hg
Low volume = < 30 mm Hg

Causes of change in volume of pulse:-

Good volume Low volume
Physiological Tachycardia
Exercise Valvular stenosis
Anxiety Shock
Pregnancy Acute massive MI
Pathological Dilated cardiomyopathy
Fever Congestion heart failure
Anaemia Peripheral vascular disease
Beri beri
Thytoxicosis
AV shunts
Aortic regurgitation
Mitral regurgitation

Character:
Normal character:

Starts with rapid rise, has a rounded peak then has a rapid fall.

1. Anacrotic pulse (Parvus et tardus):

 Also known as:Pulses tardus
o Small volume, slow rising (well sustained) and late peak
o Aortic stenosis

2. Pulses parvus:
o Low volume but ill sustained pulse
o Mitral stenosis

3. Pulses alterans:
o Alternating small and large volume pulse in regular rhythm
o Congestive Heart Failure(left), dilated cardiomyopathy

4. Pulses paradoxus:
o Normally pulse volume increases during expiration and decreases during
inspiration
o When the rise or fall during expiration and inspiration respectively is more than
10 mm Hg it confirms pulses paradoxus
o Cardiac tamponade
o Constrictive pericarditis
o Acute severe asthma
5. Dicrotic pulse:
o Single pulse wave with two peaks. One peak palpable in systole and other peak
palpable in diastole.
o Dilated cardiomyopathy
o High grade fever: typhoid fever

6. Pulsus bisferiens:
o Single wave with two peaks in systole.
o Aortic Regurgitation
o Aortic Stenosis + Aortic Regurgitation
o Hypertrophic obstructive cardiomyopathy

7. Pulsus begiminus:
o Regularly irregular pulse with a pre mature beat (extrasystole) after every
normalbeat or 3 or 4 normal beats with a pause.
o Digitalis toxicity
o Multiple unifocal ectopics with fixed pattern

8. Collapsing or water hammer or corrigans pulse:

 o Large volume pulse with rapid upstroke giving a tap to (water hammer) palpating
finger followed by a rapid downstroke producing sudden disappearance of pulse
(collapsing character)
o Aortic regurgitation
o Patent ductus arteriosus
o AV fistula

Delays:
I. Radio femoral delay:
o Delay of femoral pulse compared with radial pulse of same side
o Coarctation of aorta
II. Radio radial delay:
o Delay of left radial pulse compared to right radial pulse
o Preductal coarctation

Arterial wall:
I. Peripheral arteries become lengthened, tortuous and harder so become palpable
II. Vessel wall become stiff and hardened in old age and in hypertensive due to
arteriosclerosis and atherosclerosis so it becomes palpable

JUGULAR VENOUS PRESSURE(JVP)

Done to assess

1. The approximate mean right atrial pressure

2. The venous wave forms

Method:

 Make the patient lie down supine with head resting on pillows at an angle of 45°
 The right internal jugular veins are observed for pulsations and the highest point
ofpulsations are noted.
 Place a ruler (scale) vertical on the angle of lowis (sternal angle) and another ruler
horizontal at the level of the pulsation noted such that both the scale form a right angle
with each other.
 The point at which the right angle is formed on the vertical scale gives the JVP
Note: right internal jugular vein has no valves, is larger and straight so it gives a better
measurement than left.

Normal JVP at 45° angle = 4 – 5 cm of H2O

Mean right atrial pressure = JVP + 5 cm because sternal angle is 5 cm above right atrium.

Normal= <9cm of H2O or <8mm Hg

Difference between jugular and carotid pulsations:-

Jugular vein pulsation Carotid artery pulsation

Not palpable better visible Palpable
Diminish or obliterate on pressure No effect
Two peaks per heart beat One peak per heart beat
Decrease with inspiration No effect
Drops with upright position Unchanged
Becomes permanent with abdominal pressure No effect

Causes:-

Increased JVP Decreased JVP

Right sided heart failure Shock
Tricuspid stenosis Hypovolemia
Constrictive pericarditis Addison’sdisease
SVC obstruction (bilateral raised but non
pulsatile)

Waveform of JVP
A wave:
i. produced by right atrial contraction
ii. precedes S1

C wave:
i. produced by right ventricular pressure rise causing bulging of closed bicuspid
valve into right atrium
ii. Succeeds S1
X wave:
i. Produced by Atrial relaxation
ii. Precedes S2

V wave:
i. Atrial filling when ventricle contracts

Y wave:
i. opening of tricuspid valve
ii. Succeeds S2

Abnormalities of different waves of JVP

A wave:
 Absent:
o atrial fibrillation
 Prominent :
o Pulmonary hypertension
o Pulmonary stenosis
o Tricuspid stenosis
 Giant:
o Complete heart block
o Ventricular tachycardia

C wave:
 Not usually appreciated

X wave:
 Prominent:
o Constrictive pericarditis
 Diminished:
o Dilated right ventricle
 Absent:
o Tricuspid regurgitation

V wave:
 Prominent:
o Tricuspid regurgitation
 Diminished:
o Tricuspid stenosis

Y wave:
 Slow descent than normal:
o Tricuspid stenosis
 Fast descent than normal:
o Constrictive pericarditis
o Right side heart failure
 Absent:
o Cardiac tamponade

Kussmaul’s sign:
normally JVP decreases during inspiration but inspiratory increase in JVP is called
kussmaul’s sign caused by constrictive pericarditis

Abdominojugular reflex:
 Apply firm pressure with the palm of hand over the periumblical area for 10-30 seconds.
In normal individuals the JVP rises transiently less than 3 cm and falls even if the
pressure is continued.
 In right side heart failure it increases and remains elevated hence abdominojugular reflex
is positive.
 If pulsation are not visible at an inclination of 45° in normal individuals then
abdominojugular reflex is performed resulting in transent rise and fall in JVP confirming
normal JVP.
 When the person sits upright the pulsation are hidden behind clavicle and sternum.
 When the patient reclines at 45° the pulsation are at the level of clavicle.

PALPATION
 1. Shape of chest/precordium:

Precordium – anterior chest overlying the heart

a. Inspect the chest and precordial area.

b. Any chest deformity

Barrel shaped chest Ap diameter Is increased In COPD patients

Funnel shaped chest
(cobblers chest or pectus
excavatum)
Sternum is depressed.
Seen sometimes casuing
compression of heart and
vessels producing murmurs
(emphysema)
, may be an occupational
deformity as cobblers or may
be congenital.

Pigeon chest The sternum is displaced Seen in rickets

(keeled chest or pectus anteriorly
carinatum)
Flail chest the fractured multiple ribs
move paradoxically in the
opposite direction i.e. move in
during inspiration.

c. Any bulge or depression

Precordial bulge-Right ventricular hypertrophy in childhood.

2. Position of trachea:-
Central or midline Pulling or same side deviation Pushing of opposite deviation

Asthma Collapse of lung(atelectasis) Pleaural effusion

Bronchitis Fibrosis Pneumothorax
Lung abscess Thickened pleura Hydrothorax
Emphysema pyothorax
Consolidation

Method:

Ask the patient to extend his neck and swallow simultaneouslylook at the position of the
trachea
 3. Position of apical impulse:-
Normal position: 5 th intercostal space half inch medial to the mid clavicular line..
The position of apex beat may be displaced to the same side or the opposite side along
with the trachea when the mediastinum is shifted

Conditions in which apical impulse is not visible or not appreciated in the normal position:-

Obese person or thick chest

Apex beat is behind the rib
Dextrocardia
Hyperinflation of lungs(copd or asthma)
Large pericardial effusion

Look for apical impulse on right side also as present in dextrocardia

4. Visible pulsations
a. Neck pulsations (carotid):-
i. Systemic hypertension
ii. Coarctation of aorta
iii. Aortic regurgitation

b. Supraclavicular pulsations:-
i. Subclavial artery aneurysm
ii. Aortic regurgitation

c. Suprasternal pulsations:-
i. Coarctation of aorta
ii. Aortic regurgitation
iii. Aortic arch aneurysm

d. Aortic pulsations( Right second inter coastal space):-

i. Aortic regurgitation
ii. Aortic aneurysm
iii. Dilation of ascending aorta

e. Pulmonary pulsations:-
i. Second left intercoastal space
ii. Pulmonary hypertension
iii. Pulmonary artery dilation
 f. Parasternal pulsations:-
i. Mitral regurgitation
ii. Right ventricular hypertrophy

g. Apical pulsations:-
i. Left or right ventricular hypertrophy

h. Epigastric pulsations:-
i. Aortic aneurysm
ii. Aortic regurgitation
iii. Tumor over aorta

i. Hepatic pulsations:-
i. Tricuspid stenosis
ii. Tricuspid regurgitation
iii. Aortic regurgitation
j. Inter and infra scapular pulsations (back):-
i. Coarctation of aorta

5. Any dilated veins:

a. On chest wall : superior vena cava obstruction
b. Around shoulder: axillary or subclavian vein obstruction

6. Any other findings:

a. Sinuses or scars

PALPATION
Note:

1) Aortic area : second right intercoastal space

2) Pulmonary area: Left second intercostals area
3) Tricuspid area: left sternal border at fifth intercostal space
4) Mitral area: fifth Intercostal space half inch medical to the midclavicular line
 1. Apex beat:
Method – In sitting or lying down position, place your hand flat on the precordium
localize the intercoastal space in which the apical impulse is felt then place the ulnar
border of right hand to locate the exact position of apical impulse.

Character of apical impulse :

Heaving/sustained apical impulse Has a forceful character
Hypertension, severe aortic stenosis
Diffuse apical impulse Less forceful character
Palpable over a large area
Left ventricular dilatation (severemitral
regurgitation and aortic regurgitation)
Ischaemic heart disease
Tapping apex beat Palpable first heartsound in mitral stenosis
Double apex beat Two beats felt during each systole
Hypertrophic cardiomyopathy

Causes of shift of apical impulse

To same side To opposite side
Left ventricular hypertrophy Massive pleural effusion
Pulmonary conditions like Pulmonary conditions like
Fibrosis Pneumothorax
Collapse Hydrothorax
pneumonectomy Pyothorax

2. Parasternal heave/impulse:-
a. Palpable impulses in the lower parasternal area which lift the examiners hand
from the chest.

Method:Place your (examiner) ulnar border of right hand on the left parasternal area and
observe for the palpable impulse lift up your hand.

Causes:- Right ventricular hypertrophy:-

a. Pulmonary hypertension
b. Pulmonary stenosis

Grades of parasternal heave:

Grade 0: No lift : normal

Grade 1: Visible but not palpable

Grade 2: Visible and palpable but obliterable

Grade 3: Visible and palpable but not obliterable

3. Palpable pulsations:
a. Pulmonary pulsation:-
Method:-Place the ulnar border of right hand in the left second intercostal space
 Pulmonary hypertension
 Pulmonary artery dilation

b. Aortic pulsation :-
Method:-Place the ulnar border of right hand in the right second intercostal space
 Aortic regurgitation
 Dilation of ascending aorta

c. Epigastric pulsation:-
Method:-Place index finger below xiphistermium with the hand open and fingers
spread and press backwards and upwards
 Aortic aneurysm

4. Palpable sounds /thrills:

a. Thrills are palpable murmurs felt on the examiners hand like purring of a cat.

Method:-Thrills are palpated by putting the palm of right hand flat in the area where
thrill is suspected

Note:

1) Aortic thrill are better felt in forward leaning position

2) Mitral area diastolic thrills are better felt in left lateral position

Area Event of cardiac cycle Causes

Apical (apex of heart) Systolic
Apical (apex of heart) Diastolic
Left lower parasternal area Systolic
Carotid vessel in neck Systolic
Second right intercostal space Diastolic
Second right intercostals space Systolic
Second left intercostals space Systolic
Second left intercostals space Continuous
(systolic +diastolic)
Mitral regurgitation
Mitral stenosis
Ventricular septal defect
Aortic stenosis
Acute aortic regurgitation
Aortic stenosis
Pulmonary stenosis,
Atrial septal defect
Patent ductus arteriosus

PERCUSSION
o Useful for estimation of position and size of heart as in
o Dextrocardia
o Pericardial effusion
o Dilated cardiomyopathy

Border of heart

1) Left border
2) Upper border
3) Right border

Method:-

1) Left border: Start percussion in the third ICS from anterior axillary line towards the
sternum till the lung resonance becomes dull. Repeat similarly in the 4,5,ICS till the apex
beat and mark the left border of the heart.
2) Upper border: Percuss in the second and third ICS from above downwards till the lung
resonance becomes dull to mark upper the border of heart.
3) Right border: Percuss in the third ICS from the mid clavicular line towards the right
sterna border till the lung resonance becomes dull. Repeat the same in the remaining ICS
below till liver dullness is percussed and mark the right border of the heart.

Note:-
 i. Normally the right border of the heart is retrosternal
ii. Normal cardiac borders become disproportionate in
a. Massive pericardial effusion
b. Swelling in mediastinum

iii. Left second ICs dullness indicate: pulmonary hypertension

iv. Cardiac dullness is lost/obliterated or becomes resonant in COPD
v. Right second ICS dullness indicates aortic aneurysm

AUSCULTATION
Method : Follow a fixed pattern for auscultation with the stethoscope starting first in the right
second intercostals space (aortic area) close to the sternum then move to the left second
intercostals space close to the sternum (pulmonary area) then move to the left fifth intercostals
space (tricuspid area) close to the sternum finally to the left fifth Intercostal space half inch
medial to the midclavicular line forming a Z shaped pattern.

 Auscultation must be done with both the diaphragm and bell in all the areas
(Aortic,Pulmonary,Tricuspid,Mitral)

1. Diaphragm of stethoscope is useful for

 For High pitched sounds / murmur like
i. First heart sound
ii. Second heart sound
iii. Clicks
iv. Opening snaps
v. Rubs
vi. Systolic murmurs
vii. Early diastolic murmurs

2. Bell of stethoscope is useful for

 For Low pitched sounds and murmurs like
i. Third Heart sound
ii. Fourth Heart sound
iii. Mid diastolic murmurs
  Also auscultate over the carotids and axilla
 Identify S1, S2 at each site and observe the intensity , character and splitting of these
sounds.
 Auscultate for additional sounds and murmurs.

Importance of position of patient in auscultation

1) Sitting and lying down position
 Mid diastolic murmur (AR) or tumor polyp of atrial myxoma is better heard in
sitting position and disappears or becomes less audible in lying down position.

2) Left lateral decubitus position

 S3 , S4 and mid diastolic (M5) murmurs become louder in left lateral decubutis
position,
3) Forward leaning position
 Soft diastolic murmurs of aortic regurgitation become louder in this forward
leaning position which are usually missed.

Effect of respirationduring auscultation

1) Inspiration – Pulmonary and tricuspid (right sided murmurs) become easily audible in
held inspiration.
2) Expiration – aortic and mitral (left sided murmurs) become easily audible in held
expiration.
3) Valsalva manouvre is performed for systolic murmur of left side. (Aortic stenosis, Mitral
valve prolapse, Hypertrophic obstructive cardiomyopathy)
 Murmurs of Mitral valve prolapse, Hypertrophic obstructive cardiomyopathy increase
Where as Murmurs of aortic stenosis decrease

1) Heart sounds
First heart sound –
a. Produced due to closure of mitral and tricuspid valves (atrioventricular valves)
b. Better heard at the apex.
c. Heard as LUB

Abnormalities of the 1st heart sound-

Loud Soft Variable
Mitral stenosis Mitral regurgitation Atrial fibrillation
Tricuspid stenosis Left ventricular dysfunction Extra systoles
High cardiac output states First degree AV block Complete heart block
Atrial myxoma
Short PR interval
Atrial septal defect

Second heart sound –

a. Produced by closure of pulmonary and aortic valves (semi lunar valves)
b. Better heard at the left sternal edge
c. Louder and high pitched compared to first heart sound
d. Both components are audible the aortic component is louder than pulmonary
e. Heard as DUB

Abnormalities of the 2nd heart sound-

Loud Soft
A2 A2
Systemic HTN Calcific aortic stenosis
Aortic aneurysm Aortic regurgitation
P2 P2
Pulmonary hypertension Pulmonary stenosis

 Single S2 –
o Truncus arteriosus

 Absent A2
o Aortic stenosis
o Aortic atresia

 Absent P2
o Pulmonary stenosis
o Pulmonary atresia
o Transposition of great vessels
o Tetralogy of fallot
Third heart sound –
a. S3 produced due to rapid filling phase of ventricles
b. Low pitched
c. Better heart at the apex
d. Heard as DUM

Also Known As : triple or gallop rhythm because it resembles the sound of a galloping horse

Causes –

Physiological 3rd heart sound Pathological 3rd heart sound

Children Congestive heart failure
Young adults Congenital heart disease (ASD, VSD, PDA)
pregnant Ischemic heart disease
Mitral regurgitation
High output states

Fourth heart sound –

a. Produced due to increased resistance to ventricular filling forcing atria to contract
forcibly causing rapid emptying of atria
b. Normally heard but absent in children and adults

Causes –

1. left sided S4
o System hypertension
o Hypertrophicobstructive cardiomyopathy
o Ischaemic heart disease
o Acute mitral regurgitation

2. Right sided S4
o Right ventricular hypertrophy due to pulmonary Hypertension or pulmonary stenosis

Note: conditions in which the intensity of heart sounds decrease.

I. Thick chest wall individual
II. Obesity
III. COPD (emphysema)
2) Splitting of sounds-
a. Splitting of S1 –
o S1 has two audible components M1(mitral) and T1(tricuspid).
o M1 is louder and precedes T1
o Separated by short interval so heard as a single sound in normal subjects.
o Causes –Right bundle branch block

b. Splitting of S2 –
o S2 has two audible components A2 and P2 which are so easily audible are
widely separated.
o A2 is louder and precedes P2.
o Normal/physiological splitting –
Normally the S2 split is widest during inspiration and narrowest in
expiration.

o Wide variable splitting –

The split is wide but change during inspiration and expiration.
Causes-
 Right bundle branch block
 Pulmonary Hypertension

o Wide and fixed splitting –

Wide split but does not change during inspiration and expiration.
Causes –
 Atrial septal defect (characterstic)

o Reversed or paradoxical splitting –

The split narrows during inspiration and widens during expiration.
Causes –
 Aortic stenosis
 Hypertrophic obstructive cardiomyopathy
 Left bundle branch block
 Systemic hypertension

3) Additional sounds –
 i. Opening snap –
o High pitched, sudden early diastolic sound
o Mostly due to restricted opening of mitral stenosis and rarely tricuspid
stenosis.
o Best heard at apex in mitral stenosis and lower left sternal border in
tricuspid stenosis.
o Opening snap disappears if the stenosed valve becomes calcified or
fenestrated.

ii. Clicks –

A. Ejection clicks

o High pitched sound which follows the first heart sound in early systole
o Produced by opening of semilunar valves (aortic/pulmonary)
o Location –
 Aortic ejection clicks –
best heard at aortic area (second right intercostal space) or apex

 Pulmonary ejection clicks –

best heard at second left intercostal space.

o Causes –
Aortic ejection clicks Pulmonary ejection clicks
Aortis stenosis Pulmonary stenosis
Aortic regurgitation Pulmonary regurgitation
Dilation of aorta Dilation of pulmonary artery

B. Mid systolic clicks (non ejection) –

o High pitched sound in late systole due to prolapse of AV valve leaflets.
(mitral/tricuspid)
o Best heard at apex (mitral) and lower left sternal border (tricuspid).
o Causes –
 Mitral valve prolapse syndrome
 Tricuspid valve prolapse syndrome

iii. Pericardial rub –

  High pitched superficial scratching sound heard during both systole and
diastole
 Produced due to sliding or rubbing of the two pericardial layers
 Best heard at left sterna border
 Causes –
o Pericarditis
 Viral
 Pyogenic
 Tubercular
 Pericardial rub is not influenced by respiration

iv. Pericardial knock –

 High frequency, loud intermittent knocking diastolic sound.
 Produced due to sudden stretching of adherent pericardium in early diastolic
filling.
 Seen in constrictive pericarditis.

Murmurs –
 Murmurs are auscultatory sounds produced due to turbulence when blood flows through a
narrowed valve or large volume of blood flows through a normal valve or flow across an
abnormal orifice within the heart.
 Murmurs are described in the following headings –
o Location where it is best heard
o Timing and cause(systolic or diastolic or continues)
o Intensity (grading)
o Conduction
o Best heard with bell or diaphragm
o Variation with respiration
o Variation with position

Causes of murmurs-
 1. systolic murmurs –
a. Ejection systolic
o Aortic stenosis
o Pulmonary stenosis
o Hypertrophic obstructive cardiomyopathy
b. Mid systolic murmur
o Mitral valve prolapsed (mid systolic click +)
c. Pansystolic murmur
o Mitral regurgitation
o Tricuspid regurgitation
o Ventricular septal defect
d. Late systolic murmur
o Papillary muscle dysfunction
o Mitral valve prolapse syndrome
o Tricuspid valve prolapse syndrome

2. Diastolic murmurs
a. Early diastolic murmur
o Aortic regurgitation
o Pulmonary regurgitation (graham steells murmur)
b. Mid diastolic murmur
o Mitral stenosis
o Tricuspid stenosis
o Austin flint murmur of chronic Aortic regurgitation
o Carey coombs murmur of acute rheumatic valvulitis
c. Late diastolic or presystolic murmur
o Mild mitral stenosis

3. Continuous murmurs
o PDA
o Aortopulmonary window
o Coronary arteriovenous fistula
o Rupture of sinus of valsalva.

Location of murmurs:-
Type Location
Aortic stenosis Right second intercostal space

Pulmonary stenosis Left second intercostal space

Mitral regurgitation Apex (half inch medial to midclavicular line)

Tricuspid regurgitation Left parasternal fifth or sixth intercostal space

Ventricular septal defect Left parasternal third or fourth intercostal

space

Aortic regurgitation Right second intercostal space

Pulmonary regurgitation Left second intercostal space

Mitral stenosis Apex (half inch medial to midclavicular line)

Tricuspid stenosis Left parasternal fifth or sixth intercostal space

Patent ductus arteriosus First, second left intercostal space

Grading of murmurs –
Grade I – soft (heard in quiet room)

Grade II – soft (heard normally,noisy environment)

Grade III – easily heard no thrill

Grade IV – loud murmur with a thrill

Grade V – very loud with thrill

Grade VI – very loud heard even when stethoscope is slightly lifted away from the chest wall

Note –

 loudness of murmurs depends on the size of the orifice

 small orifice produce louder murmur
 large orifice produce soft murmur

Conduction –
 Aortic stenosis– murmur is conducted to the neck (right carotid)
 Mitral regurgitation– murmur is conducted to the axilla
 Pulmonary stenosis– murmur is conducted to the left infraclavicular area
Use of Bell/diaphragm of stethoscope –
 Bell –
o mid diastolic murmurs (Mitral stenosis,Tricuspid stenosis )
 Diaphragm –
o Ejection systole murmur (Aortic stenosis, Pulmonary stenosis)
o Early diastolic murmur (Aortic regurgitation, Pulmonary regurgitation)
o Pansystole murmur (Mitral regurgitation, Tricuspid regurgitation)

Effect of Respiration on murmur –

 Left sided murmur i.e. aortic and mitral (AR, AS, MS, MR) are better heard in held
expiration
 Right sided mumurs i.e pulmonary and tricuspid (PR, PS, TR, PS) are better heard in held
inspiration

Effect of Posture on murmur –

 Mid diastolic murmur (Mitral stenosis) is best heard in left lateral position
 Early diastolic murmur (Aortic regurgitation) is best heard in sitting and leaning forward
position

Flow/innocent murmurs –
 Soft systolic murmur due to abnormal rapid flow across a normal valve
 Seen in individuals without any cardiac abnormalities
 Benign in nature
 Seen in children, young adults and elderly.