CARDIOVASCULAR

SYSTEM
EXAMINATION

Dr. Ashish
Dhandare
 General Examination :-
Build & Nourishment.
Conscious & co-operative.
P, I, C, C, LN & Oedema.
Vital signs :- Pulse - Rate & Rhythm
BP - in R-UL in supine position.
Temp.
Anaesthesia related examination :-
1) Teeth,
2) Mouth opening, TM distance & neck movements,
3) MMP grade.
 Pallor :-
Anaemia may exacerbate angina & heart failure.
 Cyanosis :-
Bluish discolouration of skin & mucous membranes d/to
sed
quantity of reduced Hb (>4g/dl) or >30% of total Hb &
PaO2 <85% or d/to the presence of abnormal Hb pigments
in the
blood perfusing these areas.

Types of cyanosis :-
1) Central,
2) Peripheral,
 Central Cyanosis :-
Causes:-
A] sed arterial O2 saturation :-
a) High altitude ( d/to sed atm pressure),
b) V/P mismatch,
c) Anatomic shunts ( desaturated bld bypassing lungs )-
1) Cyanotic CHD,
2) Pulm AV fistula,
d) Hb with low affinity for O2.
B] Hb abnormalities :-
a) Methhaemoglobinemia (>1.5g/dl)
1) Hereditary,
2) Aquired Nitrates, sulphonamides.
b) Sulfhaemoglobinemia (>0.5g/dl),
c) Carboxyhaemoglobinemia (smokers).

In Meth-Hb-nemia Pts bld remains brown after exposing to fr

air.
But in cyanosis d/to reduced arterial O2 saturation;- Pts bld tur
red on exposure to air.
 Peripheral cyanosis :-
Causes :-
A] Reduced CO ( Reduced flow causing more O2 extraction ),
B] Cold exposure,
C] Arterial/venous obstruction,
D] MS cyanosis over malar area produces malar facies/ malar flu
 Differential cyanosis :-
Causes :-
A] Cyanosis seen only in LLs - PDA with Pul HTN with RL shunt

B] Cyanosis seen on,y in ULs ---- & Transposition of grt vessels

 Clubbing :-
Bulbous enlargement of distal partion of the digit d/to sed
periungual soft tissue.
 The normal angle bet.n nail & nail bed 160.
a/k/as Lovibond angle.

Min duration to manifest 2-3wks.

1st appears in Index finger.

 Grading of clubbing :-
I - Obliteration of the angle
& +ve fluctuation test.
II - Parrot beak appearance.
III - Drumstick appearance.
IV - Hypertrophic osteoarthropathy.

Hypertrophic osteoarthropathy :-
Painful swelling of the wrist, elbow, knee, ankle with radiogr
evidence of sub-periosteal new bone formation.
Causes :- 1) Familial / idiopathic,
2) Br. Ca, 3) Cystic fibrosis,
4) NF 5) AV malformation.
 Schamroths sign :-
When dorsum of the distal phalanges of the fingers of
both hands are approximated to each other, a Diamond
shaped gap is formed d/to the presence of the Lovibond
angle.

This gap disappears with obliteration of the angle.

 Theories of clubbing :-
A] Neurogenic Vagal stimulation vasodilation clubbing.

B] Humoural GH, PTH, Oestrogen, PGs, bradykinin vasodilata

C] Ferritin - sed ferritin Dilatation of AV anastomoses & hypertro

D] Persistent hypoxia opening of AV fistulae of terminal phalynx

E] PDGF Released 2ndary to infn in body vasodilation clubb

Latest & most accepted theory of clubbing.
 Causes of clubbing :-
A] Congenital / familial,
B] Aquired Tophaceous gout,
Local injury,
Sarcoiodosis,
Hemiplegia.
C] Pulm/ Thoracic causes Br. Ca, Metastatic lung ca, chronic br
Suppurative lung d/ses;- cystic fibrosis,
lung abscess,
empyema,
bronchiectasis.
Interstitial lung d/ses,
Long standing pulm TB,
D] Cardiovascular causes - Cyanotic CHDs,
Infective endocarditis,
Atrial myxomas,

E] GI causes Liver cirrhosis,

Ulcerative collitis,
Crohns d/s,
GI malignancy.

F] Miscellaneous Syphilis,
Acromegaly,
Thyrotoxicosis.
 Oedema :-
S.C. edema which pits on pressure cardinal feature of CHF.
Pressure appd over bony prominences.
D/to H2O & Salt retention by kidneys.
2 major mechanisms :-
I] CHF

Hypotension

Reduced renal perfusion

 Sympathetic activation & Ang-II production

Preglomerular arteriolar constriction

Reduced glomerular filtration

Reduced Na+ delivery to nephron
II] Increased Na+ reabsorption from nephron

More Imp mechanism.
Early heart failure Na+ reabsorption mainly from PCT.
As HF worsens;- Na reabsorption also from DCT & CT
d/to activation of R-A-A system.
 Salt & H20 retention expands Plasma vol

Increased capillary hydrostatic pressure

Fluid is driven out into interstitial space

Oedema.
`
 D/to effect of gravity on hydrostatic pressure

Edema develops in most dependant part.
Around ankles in ambulatory pts &
Around sacrum in bedridden pts.

In advanced heart failure, It may involve legs, genitalia &

trunk.
Transudation of fluids in pericardial space pericardial
effusion,
Transudation of fluid in peritoneal cavity ascites.
 CVS examination :-
1) Pulse,
2) BP,
3) JVP,
4) Inspection of precordium a) bony / spine abnormalities,
b) chest shape,
c) trachea central / deviated,
d) visible precordial bulge,
e) visible pulsations,
f) scars, dilated veins, sinuses.
 5) Palpation a) apex beat,
b) parasternal heave,
c) any palpable pulsations in precordial region,
d) shocks,
e) thrills.
6) Percussion,
7) Auscultation.
 Pulse :-
A pulse wave is a waveform that is felt by the finger, produce
cardiac systole which traverses the arterial tree in a peripheral d
at a rate much faster than that of the bld column.
 Assessment of pulse :-
Rate,
Rhythm,
Volume,
Character,
A-P deficit,
Cond.n of vessel wall,
R-F delay,
whether felt in all peripheral locations & symmetry.
 Radial pulse Rate & rhythm,
Carotid pulse Vol & character,
Brachial pulse BP.

Pulse can be recorde in the following way;-

Normal ---- +
Reduced ---- +/-
Absent ---- -
Aneurysmal ---- ++
 Pulse rate :-
Counted for 1 full min by palpating the radial artery.

Normal pulse rate 60-100/min.

Sinus bradycardia - <60/min.
Sinus tachycardia - >100/min.
 Causes :-
Sinus Bradycardia Sinus Tachycardia
Physiological Athlets, Physiological Infants &
children,
Sleep. Emotions,
Exercise.
Pathological Pathological
Severe hypoxia, Tachyarrhythmias,
Hypothermia, High output states,
Myxoedema, Hypovolemia,
Acute inf wall MI, Acute ant wall MI,
Raised IOP, Hypotension,
B-blockers, digoxin, Atropine, thyroxine,
 Pulse rhythm :-
Normal sinus rhythm - Regular
Young patients phasic veriations d/to Sinus arrhythmia.
A] Regularly irregular rhythm
Atrial tachyarrhythmias with fixed AV block,
ventricular bigemini, trimgemini.

B] Irregularly irregular rhythm

Atrial / ventricular ectopics,
AF,
Atrial tachyarrhythmias with variable AV block.
 Pulse volume :-
Assessed by palpating Carotid artery. ( closest to heart & least s
cted to damping & distortion in arterial tre
But PP gives accurate measurement of pulse vol.
when PP between 30-60mmHg Normal vol pulse.
<30mmHg - Small vol pulse. (Heart failure)
>60mmHg - Large vol pulse. (AR)

Pulse vol depends on SV & Arterial compliance.

 Pulse character :-
Best assessed in Carotid arteries.
 Hypokinetic pulse :-
Small weak pulse ( Small vol & narrow PP)
 Anacrotic pulse (Parvus et
Tardus):-
Parvus low amplitude
Tardus slow rising & late peak.
 Hyperkinetic pulse :-
Rapid rise
High amplitude
(Large vol & wide PP)
 Collapsing/Water-Hammer/Corrigans pulse
:-
Rapid upstroke (High SBP) d/to increased SV,
Rapid downstroke (Low DBP) d/to diastolic run off to LV / to pe
Large SV volume streching of carotid arteries aortic sinus r

reduced peripheral vasc res
 Pulsus bisferiens :-
Single pulse wave with 2 peaks in systole.
Best felt in Brachial & Femoral artery.
D/to ejection of rapid jet of
bld through aortic valve.
 Pulsus Dicroticus :-
Single pulse wave with 2 peaks one in systole & other in diasto
d/to very low SV & decreased periphearal resistance.
 Pulsus alterans :-
Alternating small & large vol pulse with irregular rhythm.
Best appreciated by palpating radial & femoral pulses.
 Pulsus bigeminus :-
A pulse wave with; Normal beat f/by premature beat
& a compensatory pause,
occuring in rapid succession caus
alteration in the strength of pulse.

Seen in Digitalis toxicity.

In pulsus alterans; compensatory pause is absent.
 Pulsus paradoxus :-
During Inspiration - sed RV Vol & Stroke Vol but;
sed LV svolume & SV.
Therefore, Fall in BP during inspiration.
When Heart constrained in a fixed cavity

Increase in RV vol during inspiration reudces the LV
compliance

More reduction in LV filling, LV-SV & SBP during inspiration.

 When the fall in BP during inspiration - >10mmHg

Pulsus Paradoxus.
 A-P deficit :-
Difference between HR & PR when counted simultaneously for

Heart beats which follow short diastolic interval

Not able to generate sufficient pressure.
Hence, not palpable at the radial artery.

Causes AF A-P deficit >10/min is most likely AF.

VPCs.
 R-F delay :-
Delay of femoral pulse compared with radial pulse.
Seen in CoA.
Peripheral pulses :-
 BP :-
The lateral force exerted by the bld column per unit area of t
vascular wall that is expressed in mmHg.
In R UL in supine position.
Measured by Sphygmomanometer.
Principle of sphygmomanometry
Turbulant flow through a partially compressed artery

Creates noises (Korotkoffs sounds)

Change in intensity correlates with systemic arterial pressures
 Korotkoffs sounds :-
5 phases;-
I 1st appearance of clear, tapping sounds.
Represent SBP.
II Tapping sounds are replaced by soft murmurs.
III - Murmurs become louder.
IV Muffling sounds.
V Disappearance of sounds.
Corresponds to DBP.
 In AR, diaspperance pt is very low.
sometimes 0mmHg.
So, Phase IV is taken as DBP.

If Korotkoffs sounds are not heard while recording.

Ask pt to raise the cuffed UL & ask to open & close the fist.
then record the BP.
 Auscultatory gap :-
Certain pt.s with HTN occaisionally;-
After initial appearance of korotkoffs sounds, the sounds disap
for sometime & then reappear again &
finally disappear at DBP.
Overestimates the DBP &
Underestimate the SBP.
Thus, palpatory method must be used to confirm.
 Dimentions of BP cuff :-
Length of the bladder twice that of width.
Avg. length of bladder - 25cms.
Air bag in the cuff extend for atleast 2/3rd of
arm length & circumference.
Mid-portion of air bag should lie over the brachial artery.
Inflate the cuff to >20mmHg above sounds disppear.
Deflate the suff @ 2-3mmHg/sec.
Manometer @ the same level of the cuff & observers eye.
 For children various cuff sizes are available.
Select the one which covers most of the arm leaving 1cm below
& 1 cm above antecubital foss
 BP in basal condition :-
Rested for 15 mins before recording,
in a quiet room,
not have consumed coffee/tea for the preceding 1 hr,
not have smoked 15 mins before recording,
not be on adrenergic stimulants,
no bladder distension.
 Normal BP recordings :-
SBP 100-140mmHg.
DBP - 60-90mmHg.
PP = SBP-DBP.
Normal PP 30-60 mmHg.
MAP Tissue perfusion pressure.
= DBP+1/3PP
or =1/3(2DBP+SBP)
Normal MAP aprrox 100mmHg.
 Postural / Orthostatic
hypotension :-
Fall of SBP >20mmHg after standing for 3 mins from lying down

BP must be recorded in lying, sitting & standing position.

Causes 1) Hypovolemia,
2) Autonomic neuropathy ( DM, Old age),
3) Heart failure,
4) AF.
 JV pressure :-
Expressed as vertical height from the sternal angle to the zone
transition of distended & collapsed IJV.

Normal approx 5cms when recorded in reclining pos at 45 an

R-IJV is selected bcoz;- larger, straighter & has no valves.

IJV is situated between 2 heads of sternocleidomastoid.

 Positioning for JV pressure :-

Lower the BP of pt,

more supine the pos.n.

Higher the BP,

more upright the pos.n.
 JVP indicator of RAP :-
The overall height of pulsating column indiactor of mean RAP.

Centre of RA is approx 5cm from the angle of Louis.

This relationship is maintained in every pos.n.
Thus RAP = Vertical ht of bld column + 5cms. (cm of H20)

mmHg = 0.736 * cms of H20.

Normal JVP value - <8cms of H20
or <6mmHg.
Causes of elevated/fall of JVP :-
Elevated JVP :- Fall in JVP :-
1) CCF, 1) Hypovolemia,
2) TS, TR, 2) Shock,
3) Constrictive pericarditis,
4) Cardiac tamponade,
5) Ascites,
6) Pregnancy,
7) Excess IVFs.
 JV pulse :-
Reflection of phasic changes in the RA.

3 +ve waves ( a,c,v) &

2 ve troughs (x,y).
 Abnormalities of JVP :-
A] a wave abnormalities :-
1) Absent a wave AF.
2) Prominent a wave PS, Pulm HTN, TS.
3) Cannon/Giant a waves - CHB, Multiple ectopics.
B] Abnormalities of x descent - 1) Prominent constr. Pericarditis
2) Absent TR (instead may be +ve)
C] Prominent v wave TR.
D] Absent y descent Cardiac tamponade.
E] False rise in JVP Polycythemia vera (sed bld vol)
Sympathetic stimulation d/to pain, anxiety,etc
 Kussmauls sign :-
Inspiratoty rise in JVP.

Normally during inspiration, there is fall in JVP.

But in constrictive pericarditis, there is rise in JVP.

Causes 1) Constrictive pericarditis (MC cause),

2) Cardiac Tamponade,
3) RV infarct or Failure.
 Abdominal Jugular Reflux :-
a/k/as Hepatojugular reflux.
Compression over right paraumbilical area or R upper abdomen
for 30 secs
Normally JVP rises transiently by <3cm
But falls later even if the pressure is continued.

But in pt.s with R/L heart failure or TR,

JVP remains elevated.

Negative in Buud-Chiari syndrome.

 Friedreichs sign :-
Rapid fall (Steep y descent) &
Rapid rise of JVP.

Seen in;- TR,

Constrictive pericarditis.
 Chest shape :-
Before commenting about chest shape, look for spine abnormal

Normal shape of chest B/lly symmetrical & elliptical in cross s

& Transverse diam > AP diam. (2:1)

Common abnormalities of shape - Barrel shaped chest,

Funnel shaped chest,
Pigeon chest.
 Barrel chest :-
Increased AP diameter.
Normal in infancy & aging.
Seen in COPD.
 Funnel chest (Pectus excavatum)
:-
Depression in lower portion of sternum.
Compression of heart & great vessels
may produce murmurs.
 Pigeon chest (Pectus carinatum)
:-
Sternum is displaced anteriorly.
AP diameter.
The costal cartilages adjacent to
protruding sternum are depressed.
 Precordial bulge :-
Preordium Anterior aspect of chest overlying the heart.
Indicates RVH presenting since childhood.
 Visible pulsations :-
A] Apical impulse Lowermost & outermost pt of max.m impulse
sternum & clavicle at which cardiac impulse can be

B] Carotid pulsations 1) Hyperdynamic states,

2) AR,
3) CoA,
4) Systemic HTN.

C] Suprasternal pulsations 1) AR, 2) CoA,

3) Thyrotoxicosis.
 D] L parasternal pulsations 1) RVH,
2) MR.

E] Supraclavicular pulsations AR.

F] Epigastric pulsations 1) AR,

2) RVH,
3) Hepatic pulsations (R lobe of liver),
4) Tumour/nodes overlying aorta.

G] Hepatic pulsations 1) TS,

2) TR,
3) AR.
 Palpation :-
General rule
Fingertips To feel pulsations,
Base of fingers Thrills,
Base of hand Heaves.
 Apical impulse :-
The lowermost & the outermost point of maximum cardiac imp
from the sternum & the clavicle at which the cardiac impulse is f
Produced by the LV & LV-ar prtion of IVS.
Normal site -
Confined to only 1 ICS.
Area of 2.5 sq.cm.
Normal duration of thrust
- <1/3rd of systole.
Analysis of apex beat :-
DIAG FROM WIKI WITH SLIGHT MODIFICATION.
 Parasternal impulse :-
Grading ( AIIMS grading ) :-
I Visible but not palpable.
II Visible & palpable & obliterable.
III Visible & palpable but not obliterable.

Seen in RV enlargement
or LA enlargement.
 RV Enlargement LA
enlargement
Volume Pressure
Overload overload MS
MR
Fast, Slow,
ill-sustained sustained
PS impulse PS impulse

LR shunts - PS
ASD, VSD
 Thrills :-
Palpable equivalents of murmurs.
 A] Carotid thrill/ Carotid shudder :- AS

B] Aortic thrill :- Systolic AS

Diastolic Acute Severe AR,
Syphilitic AR,

C] Pulmonary thrill :- Systolic PS, ASD.

Continuous PDA, Rupture of sinus of valsa

D] L lower parasternal thrill :- VSD.

E] Apical thrill :- Systolic MR.

Diastolic MS.
 Auscultation :-
Ideal stethoscope 1) well fitting earpieces,
2) Thick long tube 25 cms length,
0.325 cms diameter.
3) Diaphragm 4 cm diameter,
bell 2.5 cm diameter.
Auscultatory areas of heart :-
DIAG 4.26
 Heart sounds :-
Relative, brief, auditory vibrations of variable intensity, freque
& quality produced by closure of the heart valves.
Abnormalities of S1 :-
Soft S1 Loud S1
Regurgitant lesions Stenotic lesions are
are usually soft usually loud
MR MS
TR TS
MS/TS with High output states
calcified
valve
Obesity
 Splitting of S1 :-
Normally M1 f/by T1.
M1 & T1 separated only by 20-30ms
Hence heard as a single heart sound.
Splitting of S1 Reverse splitting of
S1
RBBB RV pacing
LV pacing RV ectopics &
LV ectopic & idioventricular
idioventricular rhythm
Abnormalities of S2 :-
Soft S2 Loud S2 Single S2
AS/PS with Loud A2 Loud P2 D/to absent
calcified A2/P2
valve Syst HTN Pulm HTN
Absent A2 -
Atheroscler
AS
osis
Absent P2-
PS, TOF.
 Splitting of S2 :-
Normally, Wide splitting of S2 Reverse splitting of
A2 f/by P2. S2
Early A2 / Late P2 Late A2 / Early P2
Dur.n between
A2 & P2 30 MR, VSD, ASD AS, HOCM
ms. RBBB LBBB
LV ectopics RV ectopics
Heard in
children LV pacing RV pacing
& young adults RV failure Syst HTN
S3 & S4 :-
Causes of S3 :-
Physiological S3 Pathological S3
Children High output states
Young adults CHD ASD, VSD,
Athlets PDA
Pregnancy MR, TR, AR
IHD
Syst HTN
Pulm HTN
 Causes of S4 :-
Whenever atria has to contract forcefully.
1) LVH,
2) HOCM,
3) Syst HTN,
 Opening Snap (OS) :-
D/to opening of AV valves.
Sound generated d/to sudden early diastolic buckling of anterio
mitral / tricuspid leaflet d/to elevated L/R atrial pressures.
OS heard;-
Over Parasternal region - Just lat to apex -
TS (MC), MS (MC),
TR, ASD. MR, PDA,

Duration of OS from A2 is inversely proportional to Severity of M

 Ejection click :-
Produced by the opening of semilunar valves.
Aortic ejection click AS. & Pulm ejection click PS.
 Pericardial knock :-
Loud, High frequency,

Diastolic sound,

in Constrictive pericarditis,

d/to abrupt halt to the diastolic filling of heart.

 Pericardial rub :-
d/to sliding of the 2 inflamed layers of the pericardium in pericard

Scratching, grating/creaking in character,

Triphasic (during mid-systole, mid-diastole & pre-systole).

Best heard along the left sternal edge in 3rd & 4th ICS.
 Tumour plop :-
Diastolic sound,
in R/L atrial myxomas with long pedicle.
 Heart murmurs :-
Series of auditory vibrations of variable intensity, quality & freque
d/to turbulance caused by increased bld flow or
d/to bld flow through a ireegular / constricted orifice.
Described in the foll.g way :-
1) Pitch (High/Low pitched)
2) Timing & character,
3) systolic / diastolic,
4) Character,
5) Area where it is best heard,
6) Intensity (Grading),
 7) Whether best heard with the bell or diaphragm,
8) Conduction of murmur,
9) Variation with respiration,
10) Posture in which murmur is best heard,
11) Variation with dynamic auscultation.

eg;- murmur of MS is best described as;-

Low-pitched, Mid-diastolic, Rumbling murmur,
with presystolic accentuation,
Best heard in Apical region,
in LL pos.n with the bell of stethoscope,
Not radiated,
Increases with isometric exercise.
Levine & Freemans grading of
murmurs:-
Systolic murmur :- Diastolic murmur :-
I Very soft (heard in quiet rm) I Very soft
II Soft II - Soft
III - Moderate III - Loud
IV Loud with thrill IV Loud with thrill
V - Very loud with thrill
(Heard with stethoscope)
VI Very loud with thrill
(Heard even when steth is slightly
away from skin)
Early systolic murmur :-
Ejection systolic murmur :-
Late systolic murmur :-
Pansystolic murmurs :-
Early diastolic murmur :-
Mid-diastolic murmur :-
 Late diastolic murmur :-
Causes :-
MS,
TS,
Atrial myxomas
Continuous murmur :-
 To & Fro murmur (Biphasic
murmur) :-
A murmur occuring through single channel,
Occupying midsystole & diastole,
does not peak around S2.
Causes AS with AR, PS with PR.
 Systolico-diastolic murmur :-
A murmur that occupies both systole & diastole,
Occurs through different channels,
does not peak around S2.
Causes VSD with AR.
 Named murmurs :-
A] Aortic valve
Gallavardin phenomenon Austin-Flint murmur

The Harsh noisy component of Low-pitched rumbling mid-di
ESM of AS, best heard at the apex,
Which is best heard at the in severe AR.
R sternal border, &
Radiated to the neck.

Cole-cecil murmur :- Murmur of AR well heard in axilla.

 B] CAREY COOMBs Murmur :- Short, mid-diastolic murmur
best heard at the apex in cases
with MS in Acute RHD.

C] Graham Still murmur :- High-pitched, Early diastolic murmur,

best heard at the left sternal border 2nd IC
during expiration in PR.

D] Carvallos sign :- Pan-systolic murmur of TR,

best heard in tricuspid area,
which becomes louder during inspiration.

E] Gibbson murmur :- Continuous machinery murmur of PDA.

 Dynamic auscultation :-
Refers to the changes in haemodynamics by physiological &
pharmacological manouvres & the effect of these manouvres on
heart sounds & murmurs.

Respiration,
Valsalva manouvre,
Standing to squatting,
Isometric exercise.
 Respiration :-
During inspiration R sided murmurs become louder &
L sided murmurs become softer or unchanged

Expiration has the opposite effect.

 Valsalva manouvre :-
Close the nose with fingers & breath out forcibly with closed mou
against closed glottis.
Phase I Phase 2 Phase 3 Phase 4
Beginning Straining phase Release phase Overshoot of
sed Intrathoracic VR ses 1st R-sided then systemic arterial
pressure R & L filling L-sided murmurs pressures &
SV. become louder. reflex bradycardia.
Transient in LV Reflex HR.
output. Most of the
murmurs softer
but;
HOCM murmur .
 Standing to squatting :-
VR & systemic arterial resistance ses

SV & arterial pressures.

Most of the murmurs become louder. But;-

Murmur of HOCM becomes softer as LV size increases d/to mor

Squatting to standing :- Opposite changes occur.

 Isometric exercise :-
Hand grip for 20-30 sec.s

sed systemic resist, VR, BP, & heart size.

Most murmurs become louder.

AS murmur softer d/to decreased pressure gradient across the

MVPS murmur delayed d/to increased ventricular volume.
Manouvre HOCM MVPS AS MR

Valsalva or or
ph 2
Hand
grip
Squattin
g
Standing or
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