Birukfgffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffffff

Seminar

1. History taking and physical examination in CVD By Dr. Zena Admasu (Assistant professor of IM, Echo-Technician) For PC - 1 Medical students at AWU - CHS March 08, 2024

2. Outline History taking in Cardiovascular disease Physical examination in Cardiovascular disease

3. Learning objective At the end of this lesson, the students should be able to: Mention the main symptoms of CVD Show techniques BP and JVP measurement Describe characters of normal and abnormal arterial pulse Show techniques of precordial examination Mention characteristic components of a murmur Examine and grade of edema

4. Cardiac cycle Ventricular filling (80% passive 20% is by atrial ejection; So a person with atrial fibrillation(no atrial contraction) can live with 80% ventricular filling ) Isovolumetric contraction Ventricular ejection; left ventricular pressure is between 0 and 120 while aortal pressure is between 80 and 120 Isovolumetric relaxation left atrium pressure is 5-8mm Hg--- mitral valve opening

5. History taking in CVD Do not use medical term in history of patient Migraine headache(history is 100% diagnostic) unilateral throbbing like headache associated with nausea, vomiting which exacelebrate by photophobia, photophobia mainly young female Patients with CVD present with one or more of the following symptoms Exertional dyspnea Orthopnea due to increased Venus return Paroxysmal nocturnal dyspnea: sever form of orthopnea( not easily relived gasping like breathing occur). Most specific for CVD. Patient wakeup from sleep. There is respiratory center depression in medulla during sleep so patient wakeup after sever congestion Palpitation( ይደነክራል ) Anginal pain(retrosternal squeezing) mostly ischemic cause

6. Cont. Hemoptysis(sever mitral stenosis, pulmonary embolism) Cough Abdominal discomfort dyspepsia like symptom (hepatomegaly compress stomach, swelling of intestine disturb digestion, ascites) Syncope– transient loss of consciousness due to transient loss of brain perfusion (if sever become stroke) Leg swelling, orthopnea is protective form facial edema Intermittent claudication--- peripheral arterial disease

7. Cont. Fatigue Platypnea– opposite of orthopnea (CLD[chronic liver disease]--- pulmonary hypertension[ hepatopulmonary syndrome]--- due to vascular distribution of lung) Bendopnea– bending give relief specially to right because mostly pulmonary edema occur at right lung so bending increase surface area of the left lungs T repopnea– improvement in tripod position Orthodeoxia means low oxygen saturation in the upright posture and improvement when lying down Orthodeoxia is same as platypnea . The difference is platypnea is about dyspnea orthodeoxia is CO2 level of blood. CO2 is increased during sleeping Dysphagia---MS---enlargement of left atrium--- compression of esophagus– difficulty of swallowing

8. Cont. Wheezing usually expiratory due to narrowing of respiratory tract intra thoracic airway obstruction eg COPD asthma if extra thoracic obstruction we call strider Decreased urine amount Weight loss or gain, etc. weight gain due to edema but lean tissue weight loss eg muscle atrophy Obesity is risk factor for heart failure but obese patients have good prognosis once HF occur because they don’t loss weight quickly called obesity paradox

9. Cont. Exertional dyspnea Dyspnea ( SOB ) is abnormally uncomfortable awareness of breathing It could also occur with non cardiac condition, non specific L evel of dyspnea by the type of activity/exertion causing dyspnea Level of dyspnea (predict mortality as well) Grade 1 - Dyspnea at supra-ordinal activities , E.g. SOB while running

10. Cont. Grade 2 - Dyspnea at ordinary activities, E.g. SOB while farming, climbing uphill Grade 3 - Dyspnea at subordinary activities, E.g. SOB while combing hair, going to the toilet Grade 4 - Dyspnea at rest Dyspnea in cardiac patients occur when ever the work of breathing is excessive due to elevated left atrial and pulmonary capillary pressure Dyspnea can predict mortality

11. Cont. C ausing transudation of fluid into the lung, requiring extra effort to ventilate the stiff lung J receptors are responsible

12. Cont. Orthopnea Dyspnea while assuming supine position due to gravitational pooling of blood to the lungs and causing severe dyspnea Quantify the level of orthopnea by the number of pillows required to alleviate dyspnea Causes of orthopnea Common cause: Left ventricular failure Other cause: bilateral pleural effusion massive ascites paralysis of diaphragm

13. Cont. Uncommon causes: Massive ascites, pregnancy, bilateral diaphragmatic paralysis, massive pleural effusion, severe pneumonia

14. Cont. Paroxysmal nocturnal dyspnea Attacks of severe dyspnea that wakes the patient from sleep so that the patient is forced to get up from sleep and gasping for breath It is because of gravitational pooling of blood to the lungs and respiratory center depression With in 1 – 3 hours of fall of sleep

15. Cont. Palpitation Palpitation is characterized by an awareness of beating of the heart Patients commonly describe ‘ pounding’ or ‘fluttering’ heart beats Palpitation may be caused by a change in the cardiac rhythm or rate , or by an increase in the force of cardiac contraction Palpitation can be intermittent or sustained and regular or irregular

16. Cont. A sk to describe their palpitations’ onset, duration, associated symptoms and the circumstances in which they occur Abrupt onset and termination after several minutes may reflect Ventricular Tachycardia or Supra Ventricular Tachycardia Gradual onset and termination of a pounding heart beat is more consistent with sinus tachycardia Patients should try to replicate the rhythm of their palpitations by tapping on a table, which helps the examiner to determine the nature of any cardiac arrhythmia

17. Cont. Leg swelling Leg swelling is a common symptom in biventricular or right-sided heart failure and mostly it is bilateral Syncope Syncope is a transient loss of consciousness resulting from cerebral anoxia , usually due to reduced cerebral blood flow Syncope may represent a simple faint or be a symptom of serious cardiac or neurologic disease

18. Cont. What is the circumstance during syncope attack ? exam On standing for prolonged periods or standing up suddenly (postural syncope ) (Normally Venus return is equal with CO when person change position from siting to standing Venus return fall--- CO fall– brain perfusion fall then syncope) , or while passing urine (micturition syncope), on coughing (tussive syncope) or with sudden emotional stress (vasovagal syncope) It may occur suddenly without warning or preceded by symptoms of faintness or pre-syncope Such as lightheadedness, dizziness, feeling of warmth, diaphoresis, nausea and tunneling of vision

19. Cont. How long does the episode last? Is it recurrent or not ? Syncope due to arrhythmia is often sudden onset regardless of the patient’s posture Exertional syncope may occur with obstruction to left ventricular outflow by AS or HOCM(commonest genetic disease of heart) Inquire about use of anti-hypertensive or anti-anginal drugs in postural syncope

20. Cont. Causes of syncope Disorders of vascular tone or blood volume A. Disorders of autonomic control of the heart and circulation ( neurocardiogenic syncope ) V asovagal syncope and vasodepressor syncope Vasovagal syncope is associated with both sympathetic withdrawal (vasodilatation) and increased parasympathetic activity (bradycardia) W hereas vasodepressor syncope is associated with sympathetic withdrawal alone.

21. Cont. B. Postural (orthostatic) hypotension Drug induced- anti-hypertensives and vasodilators Peripheral neuropathy (Diabetes, alcoholism, nutritional (vitamin B 12 deficiency)) Decreased blood volume (adrenal insuffiency , acute blood loss) C. Situational- cough, micturition, defecation, Valsalva, deglutition 

22. Cont. 2. Cardiovascular disorders A. Cardiac arrhythmia Bradyarrhythmias- sinus bradycardia, sinoatrial block, sinus arrest, sick-sinus syndrome, atrioventricular block Tachyarrhythmias- supra ventricular tachycardia with structural heart disease, atrial fibrillation with Wolff-Parkinson-White syndrome and ventricular tachycardia

23. Cont. B. Cardiopulmonary diseases HOCMP, IHD, AS , Pulmonary hypertension e.t.c 3. Cerebrovascular disease A. Vertebrobasilar insufficiency B. Basilar artery migraine

24. Cont. Angina It is kind of chest pain It is retrosterna l chest discomfort or pain with squeezing, heaviness, pressure, radiating to the left shoulder, neck, jaw, teeth and medial border of left arm, which is worsened by exertion Types of angina

25. Cont. 1 . Stable angina Characteristic r etrosternal chest discomfort persisting for less than 10 minutes , worsened by exertion and relieved by rest or nitrates 2. Angina in ACS (unstable angina) Crescendo angina- increasing severity, frequency and duration of retrosternal chest discomfort/pain E.g. Severe and recurrent angina persisting for more than 30 minutes and not relieved by rest or nitroglycerin 

26. Cont. Exam New onset angina- chest discomfort/pain started in the last one month Angina at rest 3. Others angina Differential diagnosis of chest pain mimicking angina Pericarditis- Sharp, retrosternal or left precordial and pleuritic type of chest pain, radiating to the back and trapezius ridge, which is worsened by deep breathing, coughing, sneezing and lying flat, and relieved by sitting up and leaning forward Angina not change with breathing and position

27. Cont. Esophageal spasm- Retrosternal discomfort or pain characterized by pressure, tightness or burning in quality persisting for 2-30 minutes And which may come on after eating or drinking hot or cold fluids and may be associated with dysphagia and feeding , and the pain may be relieved by nitrates P ulmonary embolism- Abrupt onset of pleuritic chest pain, which may be retrosternal and associated with shortness of breath, cough and hemoptysis

28. Cont. Aortic dissection- Abrupt onset of anterior chest unrelenting, tearing, ripping, knife-like pain radiating to the back and between shoulder blades Spontaneous pneumothorax- Sharp pain localized to one part of the chest with severe dyspnea  Intermittent claudication Patients with claudication notice pain in one or both calves, thighs, or buttocks when they walk more than a certain distance . Long claudication distance good prognoses

29. Cont. The distance walked inducing claudication is named as ‘claudication distance’. History of claudication suggests p eripheral arterial disease Smoking is major risk factor for peripheral arterial disease , and history of vascular disease is common

30. Cont. Fatigue Common symptom of cardiac disease, and may be associated with reduced cardiac output and poor blood supply to the skeletal muscles Additional history Ask about major risk factors for coronary artery disease Hyperlipidemia (familial or not, type of hyperlipidemia, on therapy or not)

31. Cont. Smoking (duration and amount of smoking in Pack-Years) Hypertension (duration of hypertension, on anti-hypertensive drugs or not, presence of target organ damage) Family history of premature CAD (1 st degree relatives (parents, siblings) < 50 years in males or < 60 years in females) DM (duration of DM, on insulin or oral hypoglycemic drugs or not, presence of chronic complications ) RHD cause cardioembolic stroke

32. Cont. CKD ( Duration, s tage, e tiology ) Ask about history of CHD : Was she/he not exerting equally with her/his peers during childhood? Ask about history of ARF in patients with CRHD (previous history of migratory joint swelling with pain, chorea, and childhood recurrent tonsillitis ) When we take history consider risk symptom and complication

33. Examination of cardiovascular system Anatomical body marks for CVE Intercostal Space Precordium Parasternal Apex Subxiphoid Midclavicular line Sternal angle Always use cardinal step of physical examination

34. Cont.. Blood pressure Blood pressure is measured by sphygmomanometer The size of BP cuff is proper if the length and width of inflatable bladder of the cuff should be about 80% and 40% of upper arm circumference respectively Technique of measuring blood pressure

35. Cont. Patients should avoid smoking or ingestion of caffeine 30 minutes before, and rest in quiet, warm room for 5 minutes Position arm of the patient so that brachial artery is at heart level Wrap the cuff securely over the arm of patient with lower border of cuff to be 2.5 cm above the antecubital crease Place the bell of stethoscope lightly over the brachial artery

36. Cont. Feel for radial artery with fingers of one hand and inflate the cuff with the other hand until the radial pulse disappears and read the pressure on the manometer and add 30mmhg to it Deflate slowly at a rate of 2-3 mmhg per second , and notice at manometer where the sound appear, muffled and disappear

37. Cont. Korotkoff sounds Phase1- the 1 st appearance of the sounds marking systolic pressure Phase 2 and 3- increasing loud sounds Phase 4- abrupt muffling of the sounds Phase 5- disappearance of the sounds marking diastolic pressure

38. Cont.

39. Cont. When Korotkoff’ sounds remain audible despite complete deflation of the cuff, take phase 4 as diastolic pressure , noticed in AR , PDA, pregnancy S hould be taken in both arms and legs at least once ; normally a difference of 5 mmhg may occur between right and left and 10mmhg between leg and arm S hould be recorded in supine and erect position to identify postural hypotension

40. Cont. Postural hypotension: Difference of SBP >20mmhg and DBP >10mmhg while assuming from supine to erect position Hypertension should be diagnosed only when a higher than normal level has been found on at least 2 or more visits after initial screening unless it is exceptionally high

41. Cont.

42. Cont. Arterial pulse The arterial pulses should be palpated for evaluation of rate, rhythm, character, volume, RFD( coarctation of aorta) and condition of the arterial vessel wall Feel for all peripheral arteries -carotid, brachial, radial, femoral, popliteal, posterior tibial and dorsalis pedis arteries in both extremities

43. Cont. Rate and rhythm When do you say normal sinus rhythm ? The origin of the pulse should be SA node Conduction should be normal pathway SA—AV– His— purkinje (WPWA congenitally left ventricle and left atrium are communicated so the electrical impulse pass the AV node and the dely.) The rate should be 60-100 The rhythm should be regular There may be respiration(fast with inspiration and late with expiration)

44. Radial artery is commonly used to assess heart rate and rhythm Technique, Compress radial artery with pads of index and middle fingers and count pulse rate for complete one minute Determine HR, Normal HR is 60 to 99 beats per minutes

45. Cont. Determine rhythm, Normal is regular Is the rhythm regular, regularly irregular or totally irregular? Regularly irregular pulse rhythm is often due to ectopic beats(premature atrial or ventricular contraction), while total irregularity of the pulse is due to atrial fibrillation (multiple right atrium fosa generate impulse but only 1 is get through AV node and the others fail to reach ventricle and artery so there may be pulse deficit) ECG is indicated to clearly characterize the arterial pulse rhythm Determine pulse deficit, normally there is no pulse deficit

46. Cont. Difference of central HR and peripheral arterial rate Often it occurs in atrial AF due to failure in conducting all central beats to peripheral arteries 2. Pulse character (amplitude and contour) Pulse character is best assessed in the carotid artery , except in collapsing pulse where radial artery is preferred

47. Cont. Technique , Place your left thumb or left index and middle fingers on the right carotid artery on the lower third of the neck , roughly at the level of cricoid cartilage NB: Avoid pressing on the carotid sinus , which lies at the level of thyroid cartilage , Compressing the carotid sinus results in asystole and SCD Characterize pulse amplitude and pulse wave contour Amplitude of the pulse correlates reasonably with pulse pressure or volume(CO)

48. Cont. Characterize contour of the pulse wave – speed of upstroke, duration of summit and speed of down stroke Normally, upstroke is smooth and rapid , the summit is smooth and rounded , and down stroke is less abrupt than upstroke Notice for variation of amplitude from beat-to-beat and with respiration

49. Cont. Pulse volume provides crude indications of stroke volume , being small in systolic HF and large in hyper kinetic heart disease (e.g. anemia, AR , PDA, pregnancy) Arterial pulse wave forms in altered cardiac hemodynamics 1. Hypokinetic pulse ( small amplitude small CO but increased velocity of upstroke-- steep ) It occurs in hypovolemia, left heart failure, constrictive pericarditis and MS

50. Cont. 2. Hyperkinetic pulse ( increase velocity of upstroke and amplitude ) Large, bounding pulse usually associated with increased left ventricular stroke volume, wide pulse pressure and reduced peripheral vascular resistance It occurs in complete AVB, AR, anemia, PDA , thyrotoxicosis and pregnancy 3. Pulsus parvus (short) et tardus (slow) ( small amplitude, slow upstroke, long s ummit duration(straight) ) Results from obstruction to LV ejection in HOCMP , AS…

51. Cont. 4. Bisferiense pulse: Rapidly and forcefully rising upstroke followed by decline in pressure and then followed by smaller and slowly rising pulse wave Two systolic peaks and it is a characteristic of AR with or without AS 5. Pulsus alternans: Alternating high and low systolic amplitude despite regular rhythm, which occurs in severely impaired LV contraction and huge Pericardial effusion

52. Cont. 6. Pulsus bigeminus (regularly irregular) Regularly altered pressure pulse amplitude following each regular beat, and caused by Premature Ventricular Contraction 7. Pulsus parvus ( normal upstroke velocity and summit, and small amplitude) Small peak pulse, commonly observed in reduced left ventricular stroke volume, narrow PP , and increased peripheral vascular resistance

53. Cont. 8. Anacrotic pulse Small volume and slow rising pulse with notched wave on upstroke and often seen in AS 9. Pulsus paradoxus Accentuated decrease in arterial pulse amplitude and systolic BP during inspiration , which is observed in cardiac tamponade and severe asthma BP during expiration is slightly larger than inspiration but the difference should not exceed 10mm Hg if it is greater than 10 then pulsus paradoxus

54. Cont. 10. Radio-femoral delay Press both radial and femoral artery at the same time and notice for RFD at femoral artery compared to radial artery, and usually observed in COA 11. Condition of the vessel wall: Thickening (cording) or tortuosity of vessel wall (arteriosclerosis) commonly detected in the arteries of elderly individuals It doesn’t indicate presence of luminal narrowing due to atherosclerosis

55. Cont. Jugular venous pressure measurement t echnique s Normally jugular veins not palpable it is intra thoracic Position the patient Elevate head of bed at 45 o to maximize visibility of the jugular venous pulsation in the lower half of the neck Turn patient’s head slightly away from the side you are inspecting Use tangential (oblique) lighting and identify the pulsation of IJV

56. Cont. Identify the highest point of pulsation of internal jugular vein Measure the vertical distance between the highest point of jugular pulsation and sternal angle with a metered ruler and then place tongue blade at an exact right angle to the ruler and read the vertical distance on the ruler The normal upper limit is 3 cm vertically above sternal angle Distance between right atrium and sternal angle is 5 cm

57. Cont. This is about 8 cm above RA, corresponding to a JVP of 8mmhg JVP > 3cm vertically above sternal angle is considered elevated

58. Cont. If the internal jugular vein pulsation is not visible, measure the vertical distance of the point above which the external jugular veins appear to be collapsed from the sternal angle Observe the amplitude and timing of the jugular venous pulsation JVP has 2 or 3 peaks (a, c, v waves) and 2 troughs (x, y waves) Clinical features to distinguish jugular from carotid artery pulsations

59. vein is not muscular so is rarely palpable

60. Cont. Types of jugular venous waves a wave indicates atrial systole(to due increased intra thoracic pressure increment during atrial contraction) c wave indicates bulging of closed tricuspid valve towards the right atrium during right ventricular systole v wave indicates atrial filling x wave indicates atrial relaxation

61. Cont. y wave indicates atrial emptying Large a wave occurs in TS , PS and PHTN Cannon a wave is observed in AV dissociation with VT or CHB(heart block) Absent a wave is observed in atrial fibrillation Sharp, deep y descent with accentuated x descent occurs in CP

62. Cont. Prominent v wave, deep y descent and obliterated x descent occurs in TR

63. Cont. Kussmaul’s sign ( because of decreased RV compliance the JVP is not dropping with inhalation= kussmaul’s sign is + ve ) # Increase rather than the normal decrease in the JVP during inspiration, which is observed in CP , right MI and severe right HF AJR or HJR reflex test: It is a n increase in JVP during firm, mid-abdominal compression for 10 sec. followed by a rapid drop in JVP of 4 cm on release Positive AJR or HJR is usually observed in congestive heart failure

64. Cont. Precordial examination Technique of precordial examination Inspection: Is there precordial bulging ? Presence of precordial bulging indicates chronicity of the cardiac disease E.g. Congenital and multivalvular heart disease in pediatrics Is the precordium active or not ?

65. Cont. Quiet(may be normal)precordium is noticed in thick chest wall, massive PE or DCMP Active(may be normal) if you can see the pulsation of one valve. If grater than 2--- hyperactive(abnormal) Is the apical impulse visible or not? If visible, determine the location in inter costal space in relation to left mid-clavicular line The apex beat is defined as the lowest and most lateral point at which the cardiac impulse can be palpated Apical impulse is due to the recoil of heart as blood is ejected Quiet precordium--- has no apical impulse

66. Cont. The normal left ventricular impulse is located at or medial to the left mid-clavicular line at the 4 th or 5 th inter costal space Down ward and laterally displaced apical impulse suggests left ventricular enlargement Technique: Localize the left 2 nd inter costal space at lateral to sternal angle Count down the interspaces, and point out the most laterally and down ward located cardiac impulse with a tip of right index finger

67. Cont. Palpation Localize and characterize point of maximal intensity and d escribe the location, amplitude and duration Is it localized or diffuse ? PMI– which valve pulsate more forcefully from the 4 valves Diffuse PMI occupies >2.5 cm in diameter, palpable between 2 nd and 4 th finger tips while off the 3 rd finger tip from the precordial area or occupies more than one interspace

68. Cont. Technique : Put the tip of index, middle and ring fingers over the site of PMI, and if you feel the impulse with tip of index and ring fingers while off the tip of middle finger, PMI is diffuse Is it sustained or not ? # apical impulse is shorter than carotid pulse. It is less than 2/3 of carotid pulse Sustained PMI occupies more than 2/3 of cardiac cycle Is it thrusting or tapping?

69. Cont. Thrusting, sustained, high amplitude impulse suggests left ventricular hypertrophy due to pressure over load (hypertension, aortic stenosis) Tapping PMI occurs in mitral stenosis( neka argo melese ) Palpable heart sounds Feel for palpable heart sounds at all valve area Parasternal and apical lift or heave

70. Cont. Technique : Put ulnar border of the hand over left sternal area and look for lift or heave Left parasternal lift suggests RVH or severe TR with giant right atrium and apical heave suggests LVH Thrill Palpable, low frequency, vibrations associated with heart murmurs

71. Cont. Technique : Palpate the apex, left upper and lower sternal border and right upper sternal border with palm of examining hand, and feel for thrill as purring of a cat Timing of the thrill is required (Is it systolic or diastolic thrill?); if the thrill coincides with the carotid pulse, it is systolic thrill

72. Cont. Percussion Percussion adds little to careful inspection and palpation with recognition of cardiac enlargement May be used to identify Cardiomegaly, Dextrocardia, Pneumothorax , COPD…

73. Cont. Auscultation Heart sounds The diaphragm and bell of stethoscope permit appreciation of high- and low-pitched auscultatory sounds respectively Diastolic murmur , s3 and s4 are low pitch Location of heart valves Cardiac apex-mitral area

74. Cont. Left lower sternal border-Tricuspid area Left upper sternal border-pulmonic area Right upper sternal border-aortic area Opening of any valve is not audible

75. Cont.

76. Cont.

77. Cont. Normal heart sounds S1 ( because of closure of AV valves) and S2 ( because of Semilunar valve closure) are well heard with the diaphragm of stethoscope There is no gap between closure of tricuspid and mitral valve. If gap present it cause T1 and M1 sound which is abnormal called splitting. During expiration A2 sound is heard earlier than P2 which is normal because left ventricle is more muscular than the right. If the gap i s long called splitting. Sometimes Pulmonary valve closed earlier than aortic in diseases that cause right ventricular hypertrophy called reverse splitting. Added heart sounds ( S3 early diastolic and S4 late diastolic) S3 and S4 are low-frequency sounds, which occur early and late in diastole respectively Use the bell of stethoscope to listen 3 rd and 4 th heart sounds

78. Cont. S3 occur due to rapid ventricular filling in early diastole, causing sudden stretching of cordea tendinea and papillary muscles S4 occurs due to vigorous atrial contraction against a non-compliant ventricle Notice presence and intensity of normal heart sounds # s2 is more intense than s1 due to muscle of ventricle Increased intensity of S1 at mitral area occurs in early MS, tachycardia and pregnancy, while reduced intensity occurs in MR

79. Cont. Increased intensity of S2 at pulmonic area occurs in pulmonary hypertension 2. Notice for the presence of added heart sound Physiologic S3 occurs in young adults <40 year and pregnancy Pathologic S3 often noticed in anemia, thyrotoxicosis and severe MR S4 is usually pathological and occurs in stiff non-compliant hypertrophied ventricle due to HHD, AS and HCM

80. Cont. Heart murmur: It results from vibrations set up in the blood stream and the surrounding heart and great vessels as a result of turbulent blood flow Murmur is longer than heart sound S1to S2 ---- systolic time S2-S1—diastolic time which is longer It can be physiological or pathological Characterizing the heart murmur Location of maximal intensity Intensity/grading of the murmur

81. Cont. Radiation(TR- epigastric MR- axilla AR-- neck) # VSD and TR murmur are same lower border hollow systole but VSD not radiate Shape (configuration) Pitch and quality   Timing Identify whether the murmur is systolic(early mid late or hollow), diastolic(early mid late hollo ) or continuous(PDA) in comparison to carotid pulse In PDA Pulmonary 15-5mm Hg aorta 120-80mm Hg blood flow is present in systolic and diastolic time so continues murmur( sh - sh ---) AR is diastolic murmur. MS is diastole.. MR is systolic

82. Cont. Timing Technique: Compress the right carotid artery at the level of cricoid cartilage, and time the murmur whether systolic or diastolic Systolic murmurs coincide with carotid pulse, while the diastolic do not Systolic murmurs Mid-systolic murmur- begin after S1 and stops before S2 e.g. Murmur of AS, PS, HOCM

83. Cont. PSM (HSM) - starts with S1 and stops at S2. “ Efud ” hollow systole because s1 is muffled and covered by murmur e.g . Murmur of MR, TR LSM- starts in mid or late systole and persists up to S2 e.g. Murmur of MVP Diastolic murmur EDM- starts after S2 and fades into silence before next S1 eg. Murmur of AR, PR MDM- e.g. Murmur of MS, TS

84. Cont. LDM (presystolic) murmur- starts late in diastole and continuous up to S1 E. g. Murmur of mitral or tricuspid stenosis in sinus rhythm Continuous murmur Begin in systole, peak at S2, and continue into all or part of diastole eg. Murmur of PDA , AVM, Pulmonary shunt

85. Cont. Grading of Intensity or loudness of a murmur Grade I- faint murmur, heard only with special efforts(like respiration) Grade II-quiet but heard murmur Grade III- Moderately loud murmur Grade IV- Loud murmur accompanied by a thrill Grade V- Very loud, heard with a stethoscope partly off the chest Grade VI- Heard with the stethoscope entirely off the chest

86. Cont. Shape (configuration) Crescendo- murmur grows louder e.g. Mid -systolic murmur of MS Crescendo-decrescendo- Murmur that grows louder and then fall e.g. Mid-systolic murmur of AS Decrescendo- murmur grows softer and slowly falls e.g. EDM of AR Plateau- murmur has same intensity throughout e.g. PSM of MR

87. Cont. Location of maximal intensity Signify origin of a murmur Radiation Signify direction of blood flow Pitch High, medium or low

88. Cont. Quality Blowing, harsh, rumbling, musical (all regurgitant murmur are blowing, all stenotic murmurs are rumbling except aortic stenosis which is harsh Special techniques to accentuate faint murmurs Squatting and standing ( Valsalva maneuver) Squatting position increases venous return, left ventricular volume and arterial blood pressure, so blood flow to all valve increases, standing do the opposite . Exception MVP and HCM when the blood flow to affected valve increases the murmur slow down

89. Cont. Hand grip exercise It increases vascular resistance Murmur of MR and AR increase with hand grip exercise Respiration Left-sided murmurs increase with expiration, and right-sided murmurs increase with inspiration

90. Cont.

91. Cont. Other heart sounds Pericardial friction rub: High-pitched scratching sound audible at any part of cardiac cycle; heard best at left lower sternal border in maintained expiration and patient leaning forward and It is observed in pericarditis. Pericardial knock: Early diastolic knock sound caused by sudden halt in blood flow into the heart during diastolic filling observed in constrictive pericarditis

92. Cont. Opening snap “ gua ” diastolic: High-pitched snapping sound heard in diastole, caused by sudden opening of early non-calcified stenosed mitral valve Characteristics of common cardiac valvular lesions Mitral stenosis : Accentuated S1; opening snap following S2; low-pitched, rumbling, grade1-4, mid diastolic murmur limited to apex, increased intensity of murmur with exercise and left lateral positioning

93. Cont. Mitral regurgitation: laterally and down ward displaced apical impulse; muffled S1; S3 sound; medium to high-pitched, blowing, soft to loud pansystolic murmur radiating to axilla or base of heart. Aortic regurgitation : Water-hammer arterial pulse with wide PP , pistil-shot at femoral artery, laterally and down ward displaced apical impulse; high-pitched, soft to loud blowing early diastolic decrescendo murmur at the 2 nd to 4 th left interspace, accentuated by expiration and leaning forward

94. Cont. Austin-Flint (mid diastolic) murmur at the apex due to back regurgitant flow; and functional systolic flow murmur at the aortic area Functional murmur—normal valve create murmur due to other cause. Eg MS like murmur in AR Thyro - toxicosis anemia PS like murur Aortic stenosis : Anacrotic arterial pulse, laterally displaced thrusting and sustained apical impulse;; low- pitched, rasping, midsystolic , crescendo- decrescedo murmur at aortic area radiating to the neck (carotid shudder)

95. Cont.. Tricuspid regurgitation : Prominent V wave of JVP; low to high-pitched, blowing, pansystolic murmur at the left lower sternal border accentuated by deep inspiration (positive caravello’s sign)  Pulmonary regurgitaion : soft to loud blowing early diastolic decrescendo murmur at the 2 nd to 4 th left interspace, murmur is accentuated during expiration and it is called Graham Steell murmur

96. Cont. Leg edema(cause is increased hydrostatic pressure) Pedal and pretibial pitting edema occurs in CHF Ankle edema of cardiac origin is usually symmetrical and worsens in the evening and improves early in the morning The mechanism is because of increased capillary hydrostatic pressure Technique : Palpate behind the medial malleolus and the distal shaft of the tibia, and dorsum of foot for pitting edema by gently compressing the area for at least 15 seconds with the thumb

97. Cont. Edema of cardiac origin is symmetrically pitting (the skin is indented and only slowly refills) Grading of edema Grade1- Pedal and pretibial edema Grade 2- Edema involving leg and thigh Grade3- Edema involving abdominal wall and sacrum Grade 4- Anasarca (including peritoneum, pleura, and face)

98. .