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DYNAMIC AUSCULTATION

DYNAMIC AUSCULTATION. Dr.G.Gnanavelu Reader in Cardiology Madras Medical College, Chennai 3. DEFINITION. ‘Technique of altering circulatory dynamics by means of respiration and variety of physiological and pharmacological maneuvers and determining their effects on heart sounds and murmurs’.

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DYNAMIC AUSCULTATION

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  1. DYNAMIC AUSCULTATION Dr.G.Gnanavelu Reader in Cardiology Madras Medical College, Chennai 3

  2. DEFINITION ‘Technique of altering circulatory dynamics by means of respiration and variety of physiological and pharmacological maneuvers and determining their effects on heart sounds and murmurs’

  3. Spontaneously occur during Normal respiration After premature beats, long pauses Myocardial ischemia May be induced by maneuvers Postural changes Muller maneuver Valsalva maneuver Isometric exercise Vasoactive agents: Amylnitrite Phenylephrine Auscultatory changes

  4. DYNAMIC AUSCULTATION Proper assessment requires • Good stethoscope • Quiet room • Cooperative patient • Bare chest • Intact autonomic function and normovolemia • Knowledge about the maneuver and the changes expected

  5. IMPORTANT REFLEXES INVOLVED IN DYNAMIC AUSCULTATION

  6. BARORECEPTOR FEEDBACK LOOP Sudden decrease in arterial pressure (abrupt standing from supine position) decreases baroreceptor firing, activating sympathetic nerves and inhibiting parasympathetic nerves. This increases cardiac output and SVR which restores normal arterial pressure

  7. (MAP – CVP) (MAP – CVP) SVR = CO = CO SVR Relationship between cardiac output, systemic vascular resistance, mean arterial pressure and central venous pressure MAP = (CO x SVR) + CVP Increasing SVR increases Mean arterial pressure at any given cardiac output, whereas decreasing SVR decreases MAP at a given cardiac output.

  8. PRELOAD AFTERLOAD STROKE VOLUME HEART RATE INOTROPY

  9. RESPIRATION • Assess changes during normal respiration • Patient should be in semiupright or sitting posture • More pronounced & consistent alterations on murmur originating from right than from left side of heart • In RV failure and PHT, no increase in venous return with inspiration, hence no inspiratory augmentation of right sided murmurs and gallops • Absence of respiratory influence is of no particular diagnostic value. • Effects of inspiration may be accentuated by Muller maneuver.

  10. POST PREMATURE VENTRICULAR CONTRACTION Vent. Filling Cardiac contractility

  11. TRANSIENT MYOCARDIAL ISCHEMIA Hemodynamic changes during spontaneous angina or induced by exercise: Increase in LVEDP Papillary muscle dysfunction Reduced stroke volume Increase in arterial pressure Auscultatory changes: Paradoxic splitting of S2 becomes obvious S4 may develop during angina Late or midsystolic murmur of Papillary muscle dysfunction may appear or gets augmented

  12. STANDING Rapid standing or sitting up from lying position or rapid standing from squatting posture results in * decreased venous return due to venous pooling in legs and splanchnic vessels leading to decreased stroke volume, decreased mean arterial pressure & decrease in heart size followed by reflex increase in heart rate & systemic resistance

  13. STANDING Auscultation is carried out immediately before and after the change in posture since effects may be quite transient persisting for only 10 – 15 heart beats If patient is unable to sit upright or stand, rapid application of tourniquets at upper thigh level may reduce venous return reproducing similar response

  14. PROMPT SQUATTING Hemodynamic changes: Increase in venous return and stroke volume increase in mean arterial pressure due to combined effect of increase in cardiac output and systemic vascular resistance due to acute compression of leg arteries

  15. PROMPT SQUATTING Examiner sits on a chair with stethoscope in place while patient is still standing to assess changes occurring within first few beats after squatting In patients unable to squat, similar circulatory changes can be produced by bending patient’s knees on his abdomen in supine position

  16. PRONE POSITION & KNEE CHEST POSITION Pericardial friction rub becomes louder

  17. VALSALVA MANEUVER Forced expiration against closed glottis Manometer method: Patient blows into the mercury manometer and maintains 40 mmHg for 15 seconds Valsalva equivalent: Patient pushes back against examiner’s hand which is pressed downward on mid abdomen. The maneuver is demonstrated and patient practices the maneuver before assessment of murmur

  18. VALSALVA MANEUVER

  19. Phase 2 : used to distinguish systolic murmur of fixed vs dynamic LVOT obstruction. (HOCM vs AS). Most other murmurs decrease in intensity Phase 4 : used to distinguish left sided from right sided murmurs. Right sided murmurs that decrease during phase 2 return to baseline intensity immediately after valsalva release. Left sided murmurs require five to ten cardiac cycles to return to baseline

  20. VALSALVA MANEUVER Mechanical and reflex changes depend on 1. level of cardiac function and effective central blood volume 2. speed and magnitude of baroreceptor responses to change in arterial pressure

  21. SQUARE WAVE RESPONSE Persistent elevation of systolic and diastolic pressure with no change in heart rate. There is no overshoot of blood pressure and no bradycardia when straining is stopped. Absence of bradycardia at the end of proceduce is the easiest sign to detect. Occurs in congestive heart failure and atrial septal defect.

  22. VALSALVA MANEUVER Apart from induced auscultatory changes Used to assess • Autonomic function • Left ventricular function Used to treat Supraventricular tachycardias

  23. ISOMETRIC EXERCISE Use calibrated handgrip device or tennis ball or rolled up BP cuff. Measure the maximum effort. Patient exerts 70 – 100% of this maximum for about 30 seconds Simultaneous handgrip using both hands Valsalva maneuver during handgrip should be avoided

  24. ISOMETRIC EXERCISE • Avoid in those with ventricular arrhythmias and myocardial ischemia • Contraindicated in recent myocardial infarction, uncontrolled hypertension, cerebrovascular disease, suspected aortic dissection

  25. ISOMETRIC EXERCISE Hemodynamic changes: Significant increase in Arterial pressure Heart rate Cardiac output LV filling pressure Heart size

  26. PHARMACOLOGICAL AGENTS Commonly two agents are used • Amylnitrite - Vasodilator • Phenylephrine - Vasoconstrictor

  27. AMYL NITRITE Patient in supine position; Perform baseline auscultation 0.3 ml ampoule of Amyl nitrite placed in gauze is crushed with gloved hand near patient’s nose Warn patient that he will smell some vapors smelling like sweet almond or dirty socks Patient takes three or four deep breaths over 10 to 15 seconds Preferable to have another person to monitor systolic BP and call the level as drug takes effect Patient remains in supine position till the effect wears off

  28. AMYL NITRITE Hemodynamic changes: Initial vasodilatation leading to reduction in systemic arterial pressure Next 1- 2 mins. - Reflex tachycardia and venoconstriction lead to increase in cardiac output and velocity of blood flow

  29. AMYLNITRITE vs NITROGLYCERIN • Both lead to reduction in BP due to systemic vasodilatation • Due to reflex tachycardia and venoconstriction Amylnitrite leads to increased venous return • Venous return falls with Nitroglycerine due to venodilatation

  30. PHENYLEPHRINE Patient in supine position; Baseline auscultation Dilute 10 mg vial of Phenylephrine in 250 ml of isotonic saline 0.3 to 0.5 mg IV over 30 sec. Alternately can be given as infusion 0.1 mg/min. infusion stopped once 20 mm Hg rise in BP occurs or when intensity of murmur clearly changes It has shorter duration of action and elevates BP for only 3 – 5 mins.

  31. PHENYLEPHRINE Hemodynamic changes: Initial increase in BP for 3 – 5 mins. Followed by reflex bradycardia and decreased contractility and cardiac output Should not be used in CHF and Hypertension

  32. IMPORTANT HEMODYNAMIC CHANGES IN MANEUVERS

  33. EXPIRATION INSPIRATION S1 S2 S1 S1 S2 S1 NORMAL SPLIT A P PARADOXICAL SPLIT (LBBB, AS, HBP) P A FIXED SPILIT (ASD) A P A P PERSISTING SPILIT (RBBB, PS) A P A P RESPIRATION & SPLITTING OF S2

  34. EJECTION SOUND S1 ES AP S1 ES PA Aortic ejection sound (no change with inspiration) S1 ES A P S1 ES A P Pulmonic ejection sound (decreases with inspiration) Pulmonary vascular click (eg. PAH) – No change with inspiration

  35. S4 S1 vs SPLIT S1 vs S1 ES

  36. S2 OS vs SPLIT S2

  37. SYSTOLIC MURMUR MITRAL REGURGITATION vs TRICUSPID REGURGITATION

  38. SYSTOLIC MURMUR AORTIC STENOSIS vs MITRAL REGURGITATION vs HOCM HANDGRIP/ SQUATTING AMYLNITRITE BASELINE VALSALVA AORTIC STENOSIS MR HOCM

  39. SYSTOLIC MURMUR OF HOCM & MVP

  40. HOCM

  41. SYSTOLIC MURMURPULMONARY STENOSIS vs TETRALOGY OF FALLOT

  42. SYSTOLIC MURMURSMALL VSD vs PULMONARY STENOSIS

  43. AR MS BASELINE AFTER AMYLNITRITE Diastolic murmurAustin Flint vs Mitral stenosis Both diastolic murmurs are low frequency; best heard with bell at LV apex in left lateral position. Austin Flint : soft S1; prominent S3; Diastolic murmur of MS: Loud S1, High frequency OS

  44. CONTINUOUS MURMUR VENOUS HUM Compression of neck veins, Turning head to one side PATENT DUCTUS ARTERIOSUS

  45. Thank you

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