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Cardiovascular system examination

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CVS examination

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Cardiovascular system examination

  1. 1. CARDIOVASCULAR SYSTEM EXAMINATION Dr. Ashish Dhandare
  2. 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. 3. Pallor :- • Anaemia may exacerbate angina & heart failure.
  4. 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. 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. 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. 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. 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
  9. 9. Clubbing :- • Bulbous enlargement of distal partion of the digit d/to ↑sed periungual soft tissue.
  10. 10. • 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”.
  11. 11. • 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.
  12. 12. • 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.
  13. 13. • 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.
  14. 14. • 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,
  15. 15. 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.
  16. 16. 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 ↓
  17. 17. 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.
  18. 18. • Salt & H20 retention expands Plasma vol ↓ Increased capillary hydrostatic pressure ↓ Fluid is driven out into interstitial space ↓ Oedema. `
  19. 19. • 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.
  20. 20. 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.
  21. 21. • 5) Palpation – a) apex beat, b) parasternal heave, c) any palpable pulsations in precordial region, d) shocks, e) thrills. • 6) Percussion, • 7) Auscultation.
  22. 22. 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.
  23. 23. 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.
  24. 24. • Radial pulse – Rate & rhythm, • Carotid pulse – Vol & character, • Brachial pulse – BP. • Pulse can be recorde in the following way;- Normal ---- + Reduced ---- +/- Absent ---- - Aneurysmal ---- ++
  25. 25. 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.
  26. 26. • 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,
  27. 27. 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.
  28. 28. 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.
  29. 29. Pulse character :- • Best assessed in Carotid arteries.
  30. 30. Hypokinetic pulse :- • Small weak pulse ( Small vol & narrow PP)
  31. 31. Anacrotic pulse (Parvus et Tardus):- • Parvus – low amplitude • Tardus – slow rising & late peak.
  32. 32. Hyperkinetic pulse :- • Rapid rise • High amplitude (Large vol & wide PP)
  33. 33. 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
  34. 34. 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.
  35. 35. Pulsus Dicroticus :- • Single pulse wave with 2 peaks – one in systole & other in diasto • d/to very low SV & decreased periphearal resistance.
  36. 36. Pulsus alterans :- • Alternating small & large vol pulse with irregular rhythm. • Best appreciated by palpating radial & femoral pulses.
  37. 37. 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.
  38. 38. 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. ↓
  39. 39. • When the fall in BP during inspiration - >10mmHg ↓ Pulsus Paradoxus.
  40. 40. 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.
  41. 41. R-F delay :- • Delay of femoral pulse compared with radial pulse. • Seen in CoA.
  42. 42. Peripheral pulses :-
  43. 43. 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
  44. 44. 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.
  45. 45. • 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.
  46. 46. 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.
  47. 47. 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.
  48. 48. • For children various cuff sizes are available. Select the one which covers most of the arm leaving 1cm below & 1 cm above antecubital foss
  49. 49. 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.
  50. 50. 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.
  51. 51. 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.
  52. 52. 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.
  53. 53. Positioning for JV pressure :- • Lower the BP of pt, more supine the pos.n. • Higher the BP, more upright the pos.n.
  54. 54. 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.
  55. 55. 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.
  56. 56. JV pulse :- • Reflection of phasic changes in the RA. • 3 +ve waves ( a,c,v) & • 2 –ve troughs (x,y).
  57. 57. 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
  58. 58. 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.
  59. 59. 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.
  60. 60. Friedreich’s sign :- • Rapid fall (Steep y descent) & Rapid rise of JVP. • Seen in;- TR, Constrictive pericarditis.
  61. 61. 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.
  62. 62. Barrel chest :- • Increased AP diameter. • Normal in infancy & aging. • Seen in COPD.
  63. 63. Funnel chest (Pectus excavatum) :- • Depression in lower portion of sternum. • Compression of heart & great vessels may produce murmurs.
  64. 64. Pigeon chest (Pectus carinatum) :- • Sternum is displaced anteriorly. • ↑ AP diameter. • The costal cartilages adjacent to protruding sternum are depressed.
  65. 65. Precordial bulge :- • Preordium – Anterior aspect of chest overlying the heart. • Indicates RVH presenting since childhood.
  66. 66. 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.
  67. 67. • 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.
  68. 68. Palpation :- • General rule – Fingertips – To feel pulsations, Base of fingers – Thrills, Base of hand – Heaves.
  69. 69. 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.
  70. 70. Analysis of apex beat :- DIAG FROM WIKI WITH SLIGHT MODIFICATION.
  71. 71. 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.
  72. 72. 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
  73. 73. Thrills :- • Palpable equivalents of murmurs.
  74. 74. • 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.
  75. 75. 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.
  76. 76. Auscultatory areas of heart :- DIAG 4.26
  77. 77. Heart sounds :- • Relative, brief, auditory vibrations of variable intensity, freque & quality produced by closure of the heart valves.
  78. 78. 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
  79. 79. 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
  80. 80. 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.
  81. 81. 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
  82. 82. S3 & S4 :-
  83. 83. 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
  84. 84. Causes of S4 :- • Whenever atria has to contract forcefully. • 1) LVH, 2) HOCM, 3) Syst HTN,
  85. 85. 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
  86. 86. Ejection click :- • Produced by the opening of semilunar valves. • Aortic ejection click – AS. & Pulm ejection click – PS.
  87. 87. Pericardial knock :- • Loud, High frequency, • Diastolic sound, • in Constrictive pericarditis, • d/to abrupt halt to the diastolic filling of heart.
  88. 88. 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.
  89. 89. Tumour plop :- • Diastolic sound, • in R/L atrial myxomas with long pedicle.
  90. 90. 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),
  91. 91. • 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.
  92. 92. 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)
  93. 93. Early systolic murmur :-
  94. 94. Ejection systolic murmur :-
  95. 95. Late systolic murmur :-
  96. 96. Pansystolic murmurs :-
  97. 97. Early diastolic murmur :-
  98. 98. Mid-diastolic murmur :-
  99. 99. Late diastolic murmur :- • Causes :- MS, TS, Atrial myxomas
  100. 100. Continuous murmur :-
  101. 101. 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.
  102. 102. Systolico-diastolic murmur :- • A murmur that occupies both systole & diastole, • Occurs through different channels, • does not peak around S2. • Causes – VSD with AR.
  103. 103. 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.
  104. 104. • 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.
  105. 105. 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.
  106. 106. Respiration :- • During inspiration – R sided murmurs become louder & L sided murmurs become softer or unchanged • Expiration has the opposite effect.
  107. 107. 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.
  108. 108. 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.
  109. 109. 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.
  110. 110. Manouvre HOCM MVPS AS MR Valsalva ph 2 ↑ ↑or↓ ↓ ↓or↔ Hand grip ↓ ↓ ↑ ↑ Squattin g ↓ ↓ ↑ ↑ Standing ↑ ↑ ↓ ↓or↔
  111. 111. THANK YOU

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