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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 – Pt’s bld remains brown after exposing to fr
air.
But in cyanosis d/to reduced arterial O2 saturation;- Pt’s 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 R→L shunt
B] Cyanosis seen on,y in ULs – --”-- & Transposition of grt vessels
Cardiovascular system examination
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.
• 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
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,
Crohn’s 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/Corrigan’s 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.
Cardiovascular system examination
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 (Korotkoff’s sounds)
↓
Change in intensity correlates with systemic arterial pressures
Korotkoff’s 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 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.
= 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).
Cardiovascular system examination
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,
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.
Cardiovascular system examination
Cardiovascular system examination
Cardiovascular system examination
Analysis of apex beat :-
DIAG FROM WIKI WITH SLIGHT MODIFICATION.
Cardiovascular system examination
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
Overload
↓
Fast,
ill-sustained
PS impulse
↓
L→R shunts -
ASD, VSD
Pressure
overload
↓
Slow,
sustained
PS impulse
↓
PS
↓
MS
MR
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
are usually soft
MR
TR
MS/TS with
calcified
valve
Obesity
Stenotic lesions are
usually loud
MS
TS
High output states
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
•LV pacing
•LV – ectopic &
idioventricular
•RV pacing
•RV – ectopics &
idioventricular
rhythm
Abnormalities of S2 :-
Soft S2 Loud S2 Single S2
AS/PS with
calcified
valve
Loud A2
↓
Syst HTN
Atheroscler
osis
Loud P2
↓
Pulm HTN
D/to absent
A2/P2
Absent A2 -
AS
Absent P2-
PS, TOF.
Splitting of S2 :-
• Normally,
A2 f/by P2.
• Dur.n between
A2 & P2 – 30
ms.
• Heard in
children
& young adults
Wide splitting of S2 Reverse splitting of
S2
Early A2 / Late P2 Late A2 / Early P2
MR, VSD, ASD AS, HOCM
RBBB LBBB
LV ectopics RV ectopics
LV pacing RV pacing
RV failure Syst HTN
S3 & S4 :-
Causes of S3 :-
Physiological S3 Pathological S3
• Children
• Young adults
• Athlets
• Pregnancy
• High output states
• CHD – ASD, VSD,
PDA
• 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 & Freeman’s 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 :-
Cardiovascular system examination
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 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.
• 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 –
↑sed Intrathoracic
pressure
↓
Transient ↑ in LV
output.
• Straining phase –
VR ↓ses →
↓ R & L filling →
↓SV.
Reflex ↑ HR.
•Most of the
murmurs – softer
but;
•HOCM murmur ↑.
• Release phase –
1st R-sided then
L-sided murmurs
become louder.
• Overshoot of
systemic arterial
pressures &
reflex bradycardia.
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
ph 2
↑ ↑or↓ ↓ ↓or↔
Hand
grip
↓ ↓ ↑ ↑
Squattin
g
↓ ↓ ↑ ↑
Standing ↑ ↑ ↓ ↓or↔
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Cardiovascular system examination

  • 2. 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.
  • 3. Pallor :- • Anaemia may exacerbate angina & heart failure.
  • 4. 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,
  • 5. 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.
  • 6. 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 – Pt’s bld remains brown after exposing to fr air. But in cyanosis d/to reduced arterial O2 saturation;- Pt’s bld tur red on exposure to air.
  • 7. 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
  • 8. Differential cyanosis :- Causes :- 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
  • 10. Clubbing :- • Bulbous enlargement of distal partion of the digit d/to ↑sed periungual soft tissue.
  • 11. • 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”.
  • 12. • 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.
  • 13. • 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 angle. This gap disappears with obliteration of the angle.
  • 14. • 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.
  • 15. • 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,
  • 16. D] Cardiovascular causes - Cyanotic CHDs, Infective endocarditis, Atrial myxomas, E] GI causes – Liver cirrhosis, Ulcerative collitis, Crohn’s d/s, GI malignancy. F] Miscellaneous – Syphilis, Acromegaly, Thyrotoxicosis.
  • 17. 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 ↓
  • 18. 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.
  • 19. • Salt & H20 retention expands Plasma vol ↓ Increased capillary hydrostatic pressure ↓ Fluid is driven out into interstitial space ↓ Oedema. `
  • 20. • 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.
  • 21. 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.
  • 22. • 5) Palpation – a) apex beat, b) parasternal heave, c) any palpable pulsations in precordial region, d) shocks, e) thrills. • 6) Percussion, • 7) Auscultation.
  • 23. 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.
  • 24. 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.
  • 25. • Radial pulse – Rate & rhythm, • Carotid pulse – Vol & character, • Brachial pulse – BP. • Pulse can be recorde in the following way;- Normal ---- + Reduced ---- +/- Absent ---- - Aneurysmal ---- ++
  • 26. 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.
  • 27. • 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,
  • 28. 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.
  • 29. 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.
  • 30. Pulse character :- • Best assessed in Carotid arteries.
  • 31. Hypokinetic pulse :- • Small weak pulse ( Small vol & narrow PP)
  • 32. Anacrotic pulse (Parvus et Tardus):- • Parvus – low amplitude • Tardus – slow rising & late peak.
  • 33. Hyperkinetic pulse :- • Rapid rise • High amplitude (Large vol & wide PP)
  • 34. Collapsing/Water-Hammer/Corrigan’s 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
  • 35. 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.
  • 36. Pulsus Dicroticus :- • Single pulse wave with 2 peaks – one in systole & other in diasto • d/to very low SV & decreased periphearal resistance.
  • 37. Pulsus alterans :- • Alternating small & large vol pulse with irregular rhythm. • Best appreciated by palpating radial & femoral pulses.
  • 38. 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.
  • 39. 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. ↓
  • 40. • When the fall in BP during inspiration - >10mmHg ↓ Pulsus Paradoxus.
  • 41. 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.
  • 43. R-F delay :- • Delay of femoral pulse compared with radial pulse. • Seen in CoA.
  • 45. 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 (Korotkoff’s sounds) ↓ Change in intensity correlates with systemic arterial pressures
  • 46. Korotkoff’s 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.
  • 47. • In AR, diaspperance pt is very low. sometimes 0mmHg. 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.
  • 48. 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.
  • 49. 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.
  • 50. • For children various cuff sizes are available. Select the one which covers most of the arm leaving 1cm below & 1 cm above antecubital foss
  • 51. 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.
  • 52. 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.
  • 53. 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.
  • 54. 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.
  • 55. Positioning for JV pressure :- • Lower the BP of pt, more supine the pos.n. • Higher the BP, more upright the pos.n.
  • 56. 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.
  • 57. 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.
  • 58. JV pulse :- • Reflection of phasic changes in the RA. • 3 +ve waves ( a,c,v) & • 2 –ve troughs (x,y).
  • 60. 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
  • 61. 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.
  • 62. 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.
  • 63. Friedreich’s sign :- • Rapid fall (Steep y descent) & Rapid rise of JVP. • Seen in;- TR, Constrictive pericarditis.
  • 64. 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.
  • 65. Barrel chest :- • Increased AP diameter. • Normal in infancy & aging. • Seen in COPD.
  • 66. Funnel chest (Pectus excavatum) :- • Depression in lower portion of sternum. • Compression of heart & great vessels may produce murmurs.
  • 67. Pigeon chest (Pectus carinatum) :- • Sternum is displaced anteriorly. • ↑ AP diameter. • The costal cartilages adjacent to protruding sternum are depressed.
  • 68. Precordial bulge :- • Preordium – Anterior aspect of chest overlying the heart. • Indicates RVH presenting since childhood.
  • 69. 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.
  • 70. • 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.
  • 71. Palpation :- • General rule – Fingertips – To feel pulsations, Base of fingers – Thrills, Base of hand – Heaves.
  • 72. 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.
  • 76. Analysis of apex beat :- DIAG FROM WIKI WITH SLIGHT MODIFICATION.
  • 78. 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.
  • 79. RV Enlargement LA enlargement Volume Overload ↓ Fast, ill-sustained PS impulse ↓ L→R shunts - ASD, VSD Pressure overload ↓ Slow, sustained PS impulse ↓ PS ↓ MS MR
  • 80. Thrills :- • Palpable equivalents of murmurs.
  • 81. • 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.
  • 82. 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.
  • 83. Auscultatory areas of heart :- DIAG 4.26
  • 84. Heart sounds :- • Relative, brief, auditory vibrations of variable intensity, freque & quality produced by closure of the heart valves.
  • 85. Abnormalities of S1 :- Soft S1 Loud S1 Regurgitant lesions are usually soft MR TR MS/TS with calcified valve Obesity Stenotic lesions are usually loud MS TS High output states
  • 86. 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 •LV pacing •LV – ectopic & idioventricular •RV pacing •RV – ectopics & idioventricular rhythm
  • 87. Abnormalities of S2 :- Soft S2 Loud S2 Single S2 AS/PS with calcified valve Loud A2 ↓ Syst HTN Atheroscler osis Loud P2 ↓ Pulm HTN D/to absent A2/P2 Absent A2 - AS Absent P2- PS, TOF.
  • 88. Splitting of S2 :- • Normally, A2 f/by P2. • Dur.n between A2 & P2 – 30 ms. • Heard in children & young adults Wide splitting of S2 Reverse splitting of S2 Early A2 / Late P2 Late A2 / Early P2 MR, VSD, ASD AS, HOCM RBBB LBBB LV ectopics RV ectopics LV pacing RV pacing RV failure Syst HTN
  • 89. S3 & S4 :-
  • 90. Causes of S3 :- Physiological S3 Pathological S3 • Children • Young adults • Athlets • Pregnancy • High output states • CHD – ASD, VSD, PDA • MR, TR, AR • IHD • Syst HTN • Pulm HTN
  • 91. Causes of S4 :- • Whenever atria has to contract forcefully. • 1) LVH, 2) HOCM, 3) Syst HTN,
  • 92. 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
  • 93. Ejection click :- • Produced by the opening of semilunar valves. • Aortic ejection click – AS. & Pulm ejection click – PS.
  • 94. Pericardial knock :- • Loud, High frequency, • Diastolic sound, • in Constrictive pericarditis, • d/to abrupt halt to the diastolic filling of heart.
  • 95. 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.
  • 96. Tumour plop :- • Diastolic sound, • in R/L atrial myxomas with long pedicle.
  • 97. 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),
  • 98. • 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.
  • 99. Levine & Freeman’s 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)
  • 107. Late diastolic murmur :- • Causes :- MS, TS, Atrial myxomas
  • 109. 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.
  • 110. Systolico-diastolic murmur :- • A murmur that occupies both systole & diastole, • Occurs through different channels, • does not peak around S2. • Causes – VSD with AR.
  • 111. 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.
  • 112. • 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.
  • 113. 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.
  • 114. Respiration :- • During inspiration – R sided murmurs become louder & L sided murmurs become softer or unchanged • Expiration has the opposite effect.
  • 115. 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 – ↑sed Intrathoracic pressure ↓ Transient ↑ in LV output. • Straining phase – VR ↓ses → ↓ R & L filling → ↓SV. Reflex ↑ HR. •Most of the murmurs – softer but; •HOCM murmur ↑. • Release phase – 1st R-sided then L-sided murmurs become louder. • Overshoot of systemic arterial pressures & reflex bradycardia.
  • 116. 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.
  • 117. 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.
  • 118. Manouvre HOCM MVPS AS MR Valsalva ph 2 ↑ ↑or↓ ↓ ↓or↔ Hand grip ↓ ↓ ↑ ↑ Squattin g ↓ ↓ ↑ ↑ Standing ↑ ↑ ↓ ↓or↔