• Bluish discolouration of skin & mucous membranes d/to
quantity of reduced Hb (>4g/dl) or >30% of total Hb &
PaO2 <85% or d/to the presence of abnormal Hb pigments
blood perfusing these areas.
• Types of cyanosis :-
Central Cyanosis :-
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) –
2) Aquired – Nitrates, sulphonamides.
b) Sulfhaemoglobinemia (>0.5g/dl),
c) Carboxyhaemoglobinemia (smokers).
• In Meth-Hb-nemia – Pt’s bld remains brown after exposing to fr
But in cyanosis d/to reduced arterial O2 saturation;- Pt’s bld tur
red on exposure to air.
Peripheral cyanosis :-
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 :-
A] Cyanosis seen only in LLs - PDA with Pul HTN with R→L shunt
B] Cyanosis seen on,y in ULs – --”-- & Transposition of grt vessels
• 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.
• Schamroth’s 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
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,
C] Pulm/ Thoracic causes – Br. Ca, Metastatic lung ca, chronic br
Suppurative lung d/ses;- cystic fibrosis,
Interstitial lung d/ses,
Long standing pulm TB,
• 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 :-
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
• 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 &
Transudation of fluids in pericardial space – pericardial
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,
• 6) Percussion,
• 7) Auscultation.
• 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 :-
• 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.
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,
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
• Parvus – low amplitude
• Tardus – slow rising & late peak.
• 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
More reduction in LV filling, LV-SV & SBP during inspiration.
• When the fall in BP during inspiration - >10mmHg
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.
R-F delay :-
• Delay of femoral pulse compared with radial pulse.
• Seen in CoA.
• 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 (Korotkoff’s sounds)
Change in intensity correlates with systemic arterial pressures
Korotkoff’s sounds :-
• 5 phases;-
I – 1st appearance of clear, tapping sounds.
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.
So, Phase IV is taken as DBP.
• If Korotkoff’s 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 korotkoff’s 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 & observer’s 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.
• Normal MAP – aprrox 100mmHg.
Postural / Orthostatic
• 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,
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
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,
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
Kussmaul’s 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.
Friedreich’s sign :-
• Rapid fall (Steep y descent) &
Rapid rise of JVP.
• Seen in;- TR,
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,
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.
• 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.
Causes of S3 :-
Physiological S3 Pathological S3
• Young adults
• High output states
• CHD – ASD, VSD,
• MR, TR, AR
• Syst HTN
• Pulm HTN
Causes of S4 :-
• Whenever atria has to contract forcefully.
• 1) LVH,
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,
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,
Increases with isometric exercise.
Levine & Freeman’s grading of
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)
To & Fro murmur (Biphasic
• 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 COOMB’s 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] Carvallo’s 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.
• Valsalva manouvre,
• Standing to squatting,
• Isometric exercise.
• 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 –
Transient ↑ in LV
• Straining phase –
VR ↓ses →
↓ R & L filling →
Reflex ↑ HR.
•Most of the
murmurs – softer
•HOCM murmur ↑.
• Release phase –
1st R-sided then
• Overshoot of
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
↑ ↑or↓ ↓ ↓or↔
↓ ↓ ↑ ↑
↓ ↓ ↑ ↑
Standing ↑ ↑ ↓ ↓or↔