History, Symptoms and Physical Examination in Cardiovascular Disease.ppt

cardiology physical examination

1. 1
History, Symptoms and Physical Examination in History, Symptoms and Physical Examination in
Cardiovascular DiseaseCardiovascular Disease
Assoc. Prof. Özcan BAŞARAN
Muğla Sıtkı Koçman University
Faculty of Medicine Cardiology Department

2. 2000-2006 İstanbul Uni Medical Faculty
2007-2011 Koşuyolu E&R (Cardiology)
2012- 2020 Muğla E&R (Cardiologist)
2020- Muğla Uni Medical Faculty
Assoc. Prof. Özcan Başaran

3. Residency work hours and health care system efficiency
standards have severely restricted the time and expertise
devoted to the mentored cardiovascular examination.
In turn, less attention to bedside skills has increased the
use of noninvasive imaging, including the use of handheld
ultrasound.
Braunwald's Heart Disease:
A Textbook of Cardiovascular Medicine

4. TURKEY
Outpatient clinic
Mean time for a patient : 10 min
Mean number of patient Daily: 50 patients
How to perform
physical examination?

5. Today in Cardiology
Inspection Palpation
Percussion Auscultation

6. Do we need to know
Jugular venous waves

7. Touching patients reminds to try to remember to treat the
patients as well
 as their medical problems and physical findings
the essence of doctoring: using science and technology in
concert with the human skill of listening to determine what ails a
patient (Markel H.
 
N Engl J Med 
354:551-553, 2006). It is too
early to relegate the stethoscope, and the rest of the physical
examination, to the museum shelf.
Medicine is learned by the bedside and not in the classroom. Let
not your conceptions of disease come from words heard in the
lecture room or read from the book. See, and then reason and
compare and control,” Osler told his students. “But see first.”
 
Physical Examination, Diagnostic Imaging,
and Medical Errors

9. 9
Anamnesis
•The beginning of patient-physician relationship
•Communication skills, patience, attention
•Patients identity
•Complaint
•History
•Past medical history
•Family History

10. 10
Anamnesis
•Name-Surname: Age: Birth Place: Job:
•Complaint
•History
•Past Medical History
•Hypertension
•Diabetes mellitus
•Hypercholoesterolemia
•Smoking, alcohol
•Acute rheumatic fever
•Trauma or operation
:
•Family History
•Hypertension
•Diabetes mellitus
•Hypercholoesterolemia
•Coronary artery disease
•Congenital heart disease

11. Cardiovascular Signs and Symptoms
•Chest discomfort
•Dyspnea
•Fatigue
•Edema
•Palpitations
•Syncope

12. 12
Chest Pain (Angina Pectoris)
•Three characteristics of Angina
•Substernal discomfort
•initiated by exertion or stress
•relieved with rest or sublingual nitroglycerin.
•Atypical angina: If two characteristics present
•Non-anginal chest pain: If no or one characteristic
present

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Differential Diagnosis
1. Coronary artery disease
2. Other cardiovascular conditions
a) Ischemia related
1) Aort stenosis
2) Hypertrophic Obstructive Cardiomyopathy
3) Hypertension
4) Pulmonary Hypertension
5) Aort insufficiency
6) Anemia, hypoxia
b) Non-ischmemic conditions
1) Aort dissection
2) Pericarditis
3) Mitral valve prolapsus
3. Gastrointestinal conditions:
a) Esophagus spasm
b) Esophageal refux
c) Esophageal rupture
d) Peptic ulcus
4.Psychogenic conditions:
a) Anxiety
b) Depression
c) Cardiac psychosis
d) Personal benefit
5.Neurogenic, musculoskeletal causes
a) Thoracic outlet syndrome
b) Degenerative joint disease in the
cervical / thoracic spine
c) Costochondritis
d) Herpes zoster
e) Chest wall pain and tenderness
6.Pulmonary causes
a) Pulmonary embolism with or without
pulmonary infarction
b) Pneumothorax
c) Pneumonia including the pleura

14. 14
Chest Pain (Angina Pectoris)
•Anginal pain is usually felt retrosternal or slightly to the
left of the midline, below or behind the sternum.
•It may rarely be an isolated pain under the left breast, in
the cardiac apex.
•Myocardial ischemia pain tends to spread from both sides
to the chest and arms (more often the left arm) and the
neck and lower jaw.
•Sometimes it can spread to the posterior and occipital
bone. Pain in the arms, passing through the ulnar and
flexor side of the wrist, often radiating to the ulnar fingers
•While pain is rarely felt only in the arm, it can sometimes
start in the arm and spread to the chest.
•The body language used by the patient to describe or
indicate the location of the pain can also provide
information about the etiology. It is very typical to make a
fist and point the front of the sternum (Levine's sign).

15. Dr. Samuel A. Levine (1891-1966)

17. Differantial Diagnosis of Chest Pain
•5 Major Diseases
– Pulmonary Embolism
–Aort Dissection
–Esophageal Rupture
–Pneumothorax
–Acute Coronary Syndrome

18. Common features

22. Stable Angina Pectoris
•Coronary artery disease
•Aort stenosis
•Hypertrophic cardiomyopathy
•Hypertension
•Mitral insufficiency
•Mitral stenosis
•Mitral valve prolapsus

23. 23
Shortness of Breath (Dyspnea)
Dyspnea Difficult and tiring breathing
Uncomfortable awareness of the person's breathing.
There are 5 forms of shortness of breath
Exercise dyspnea
Orthopnea
PND
Resting dyspnea
Acute pulmonary edema

24. 24
Sudden onset dyspnea
•Pulmonary embolism
•Pneumothorax
•Acute pulmonary edema
•Pneumonia or
•Possibilities of airway obstruction should be considered.

25. 25
Chronic developing dyspnea
•Chronic CHF
•Pregnancy
•COPD
•Lack of physical condition
•Obesity
•Pleural effusion should not be ignored.

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Dyspnea
Inspiratory dyspnea: Usually upper airway obstruction
Expiratory dyspnea: Upper airway obstruction
Exercise dyspnea: Heart failure, COPD
Resting dyspnea:
Pneumothorax
Pulmonary embolism
Pulmonary edema or
Can be emotional & psychogenic

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Orthopnea
•It develops due to the increase in hydrostatic pressure in the lung while lying
down.
•Although it is most common in heart failure, it can also be seen in COPD.
•It occurs when intravascular volume accumulated in the lower extremities
due to gravity joins the venous circulation in the lying position and
redistribution in the lung.
•Its severity is determined by the number of pillows.
•It develops rapidly and when awake in a short time such as 1-2 minutes.

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Bendopnea
•In 2014, Jennifer T. Thibodeau et al. made a new definition: BENDOPNEA
•Some CHF patients describe shortness of breath when leaning forward (or
bending): for example, when leaning forward and putting their shoes on the
floor. This condition has been identified as BENDOPNEA.
•As a result of the study conducted by Jennifer T. Thibodeau et al. Consisting
of 102 patients with systolic HF, 28% of CHF patients were found to have
Bendopnea.
•The authors explain this situation with the increase in ventricular filling
pressures when leaning forward.
Thibodeau JT et al. Characterization of a novel symptom of advanced
heart failure: bendopnea. JACC Heart Fail. 2014 Feb;2(1):24-31.

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Paroxysmal Nocturnal Dyspnea
•Often develops 2-3 hours after going to
bed during sleep and usually improves
when getting up and sitting.
•Dyspnea usually does not recur when the
patient goes back to sleep.
•Attacks can be mild or sometimes progress
to the development of pulmonary edema.
•Frequent sweating and wheezing.

30. 30
PND pathophysiology
Central blood volume increases while lying flat.
Slow resorption of interstitial fluid
Increase in thoracic blood volume and increase in
diaphragm
Decrease in adrenergic support during sleep
Normal nocturnal depression of the respiratory
center.

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Dyspnea Differential Diagnosis
(Cardiac? Pulmonary?)
•Patients with COPD may also wake up with dyspnea at night. However,
cough and expectoration often precede dyspnea. There is often a history of
smoking, sputum, and wheezing. They relax after releasing secretions rather
than sitting position.
•The reduction of dyspnea with bronchodilators and corticosteroids suggests
bronchial asthma, and its decrease with diuretics and digitalis suggests HF.
•Dyspnea is relieved by sitting and standing up in HF (orthopnea). It is
relieved by expectoration in COPD.

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Cough
•Non-productive cough that comes with effort or at rest may be related to HF-
related pulmonary congestion.
•In cardiac dyspnea, first dyspnea, then cough,
•In pulmonary dyspnea, first cough and then dyspnea develop.
•While pink and foamy sputum is seen in cough that belongs to acute
pulmonary edema
•The sputum of chronic bronchitis is usually white and mucous.
•The sputum of pneumonia is often dark yellow, and that of pulmonary
infarction is bloody, as in lung cancer and brochiectasis.

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Hemoptysis
•Removal of blood from the respiratory tract by mouth
(cough with blood)
•Mechanisms of hemoptysis
•Leakage of erythrocytes from congested vessels
(Pulmonary edema),
•Rupture of dilated endobronchial vessels (Mitral stenosis)
•Hemorrhage or necrosis to the alveoli (Pulmonary
infarction)
•Ulceration and accident of the bronchial mucosa
(Tuberculosis)
•Vascular invasion (Malignancy),
•Treakea bronchial mucosa damage and mucosal necrosis
(bronchiectasis) caused by persistent cough.

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Cardiac Edema
Mechanism: Increased total body fluid, increased hydrostatic pressure,
pushing water and salt out of the vessels and collecting in the interstitial
area (not related to plasma protein content or lymphatic obst.)
It is a common symptom or finding of right or left HF.
At least 5 liters of fluid retention is required for edema to occur.
Cardiac edema is usually symmetrical. It moves from the bottom up. It is
localized in the sacral region in hospitalized patients.
If the edema is localized in the legs and maximizes towards the evening,
it is CHF or bilateral chronic venous insufficiency.

36. 36
Fatigue
•Not a specific symptom of heart disease.
•Anemia, thyrotoxicosis and all chronic diseases (inflammatory
mediators) can cause fatigue and weakness.
•Heart failure associated weakness / fatigue:
•Low cardiac output
•Congestion
•Secondary causes (anemia, electrolyte imbalance due to diuretics)

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Palpitation
•The feeling of heart beats.
•All kinds of rhythm problems (sinus tachycardia, atrial fibrillation,
supraventricular tachycardia, atrial / ventricular extrasystole, AV
block) are the cause of palpitations.
•In cases of early beats (extrasystole), it is the feeling of pause and
badness in the patient's heart due to the length of the compensatory
pause period, which is uncomfortable.

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Palpitation

40. 40
Palpitation Causes
AV block or sick sinus syndrome
Palpitations felt in slow heart rates
SVT or paroxysmal AF
Sudden onset and end of palpitation
Sinus tachycardia or anxiety
A gradual starting may be due to sinus tachycardia or
anxiety
Sinus tachycardia
The rate of tachycardia is 100-140 bpm.
Atrial flutter 150 beats / min.
PSVT 160 beats/min.

41. 41
Palpitation
Supraventricular tachycardia
Sinus rhythm

42. 42
Syncope
•Cardiac syncope is a temporary spontaneous posture and temporary
loss of consciousness as a result of insufficient cerebral blood flow
due to a sudden decrease in cardiac output.
•The sensation of presyncope is that the patient feels badness and
weakness and does not lose consciousness although his posture
reaches the point of deterioration.
•Short-term convulsion can be observed in syncope that develops with
cardiac arrhythmia.
•
•Cardiogenic syncope may be incontinent; but presence of aura,
constant tonic-clonic movements, tongue biting, confusion or sleepy
appearance; It is more characteristic of syncope due to CNS disorder.
•Conversely, after the arrhythmia returns to normal in cardiac
syncope, consciousness opens suddenly.

43. 43
Medical History
•Coronary artery disease risk factors
•Age (M> 45, F> 55)
•Male gender
•Diabetes mellitus
•Hypertension
•Hypercholesterolemia (High LDL, Low HDL)
•Smoking
•Family history of early atherosclerosis
•History of rheumatic fever,
•Habits (smoking, alcohol, parenteral substance, etc.)
•Medications used
•Chronic diseases / previous operations / allergy history

44. 44
A history of ARF (acute rheumatic fever) can be helpful in explaining
the cause of a murmur detected.
Cardiac operation / trauma history: may be the cause of constrictive
pericarditis, thoracic aortic aneurysm, A-V fistula and other cardiac
injuries.
In people with valvular disease, dental practices or other diagnostic
and therapeutic procedures increase the likelihood of infective
endocaditis.
Medical History

45. 45
Family History
•Family history is an important risk factor in congenital heart diseases.
(congenital diseases such as ASD, VSD, PDA in family members)
•The patient's mother's history of rubella in the first few months of
pregnancy increases the possibility of PDA, pulmonary valve stenosis,
pulmonary artery coarctation and ASD.
•Early coronary artery disease in the family
•The presence of genetic diseases in the family.
•Mitral valve prolapse
•Hypertrophic cardiomyopathy
•Dilated cardiomyopathy
•Marfan syndrome
•Long QT syndrome

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PHYSICAL EXAMINATION

47. 47
Cardiovascular Physical Examination
1. Cardiac Examination
2. Vessel Examination
•Arteries (pulse examination)
•Carotid, temporal, axillary, brachial, radial, femoral,
popliteal, tibialis posterior, dorsalis pedis
• Veins (Juguler vein distention)

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Physical Examination
1. Inspection
2. Palpation
3. Percussion
4. Auscultation

49. 49
1.Inspection
•General appearance (tachypnea, anxiety, depressive, confusion etc.)
•Syndromic Type (Down, Turner)
•Venous distention, pallor, cyanosis, clubbing, joint swelling
•Apex beat  Shift to the left (Cardiomegaly)
•Right ventricular beat  (Right ventricular hypertrophy)
Cardiovascular Physical Examination

50. 50
1.Inspection
•Chest pain, is it relaxed with resting (Stable angina pectoris) or restless
(MI)? Sitting upright (CHF) or leaning forward (Pericarditis)?
•Is there a vibration in the patient's body with a heartbeat or is there a
Corrigan pulse (AR, AV fistula, AV complete block)?
•Does the patient have significant weight loss, malnutrition, cachexia
(CHF)?
•Do you have obesity and cyanosis (Picwickian Syndrome)?
•Is there abdominal localized obesity (If waist / hip ratio is> 0.85, it is
pathological. Normal is <0.7) If so, DM and CAD should be investigated.
•Are there any truncal obesity, moon face, thin extremities (Cushing's
syndrome)?
Cardiovascular Physical Examination

51. 51
1.Inspection
Congenital heart disease related syndromes
•Marfan syndrome: Skeletal anomalies such as tall, long fingers, narrow
palms, kyphoscoliosis, pectus excavatum or carinatum. The legs are
disproportionately long and have an abnormal upper-lower body ratio
(0.85). Arm span may exceed length. Bilateral subluxation of the lens,
MVP, MR, AR, aortic root width, or aortic dissection are common.
•Turner and Klinefelter syndromes: Low hairline, low ears, deafness, small
chin, short and webbed neck. In addition, Turner syndrome also has short
stature, large nipples and broad chest wall, epicantal folds, large eyes,
pigmented moles, ptosis, clinodactyly, and short fifth finger. Aortic
coarctation, AS and HCM are common.
Cardiovascular Physical Examination

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1.Inspection
Skin manifestations of infective endocarditis:
•Osler nodules: reddish purple, tender, typically located at the distal end of
the finger or toe.
•Janeway spots: hemorrhagic but not sensitive; they are found on the
palms or soles.
•Splinter hemorrhages: It consists of black and fine lines observed in the
distal 1/3 of the nail.
Cardiovascular Physical Examination

53. 53
2. Percussion
•Determination of heart size (matity)
•Echocardiography gold standard
Cardiovascular Physical Examination

54. 54
3. Palpation
•Apex hit (Location, Intensity)
•Right ventricular beat
•Vibrations (thrill)
Murmurs of intensity> 3/6 generate vibration
Cardiovascular Physical Examination

55. PALPATION
•Apical zone (left ventricle)
•Left parasternal zone
(right ventricle)
•Pulmonary area
•Aortic area
•Sternoclavicular joint area
•Epigastric region

56. 56
3. Palpation: PULSE EXAMINATION
•Pulsus Filiformis: It is the feeling of the pulse fast and weakened (like a
thread) in the fingers. Its presence reminds shock state.
•Pulsus Alternans: Strong and weak pulses that alternate regularly. If the
difference is> 20 mmHg, it can be palpated. Otherwise, a
sphygmomanometer is needed. Seen in CHF
•Pulsus Parvus Et Tardus: Low amplitude that reaches the systolic peak late
and the duration at the top is prolonged. It is common in moderate or severe
valvular AS.
Cardiovascular Physical Examination

57. 57
3. Palpation: PULSE EXAMINATION
•Collapsing pulse: is used in cases where the arterial pulse wave decreases
rapidly after reaching its peak.
•Quincke pulse: It is the name given to the small pulsations that can be seen in
the nail bed of people who have a hyperdynamic arterial beat for any reason,
including AR.
•Water-hammer pulse: It develops due to rapid excretion of an increased
blood volume from the left ventricle in hyper kinetic conditions due to
increased cardiac output. Pulse pressure increased, and peripheral artery
resistance decreased.
Cardiovascular Physical Examination

58. Normal Pulse
•Dichrotic notch corresponds to component S2
(A2)
•Pulse examination: Speed, rhythm, fullness
and overall character
A2
Dichrotic
notch

59. Pulsus alternans
–The amount of muscle involved in the contraction
of the myocardium is different with each beat
–Strong and weak pulses alternate
–Found in decompensated heart failure
–But also preload and afterload changes can cause

60. Pulsus paradoxus
–Exaggeration in systolic blood pressure difference in expiration-inspiratory (TA
decreases more in inspiration)
–REASONS
•Cardiac tamponade,
•COPD, acute asthma attack,
•massive pulmonary embolism,
•right vent. MI,
•heart failure,
•tension pneumothorax, pregnancy,
•obesity and rarely constrictive pericarditis
–MECHANISM
–Increased right heart volume in inspiration decreases the diastolic filling of left
ventricle via septum. The left ventricle stroke volume decreases.
–Pooling of blood in the lung during inspiration decreases left ventricle preload

61. Wikipedia
pulsus paradoxus
Pulsus paradoxus, also paradoxic pulse or paradoxical pulse, is an
abnormally large decrease in stroke volume, systolic blood pressure
and pulse wave amplitude during inspiration. The normal fall in
pressure is less than 10 mmHg. When the drop is more than 10
mmHg, it is referred to as pulsus paradoxus. Pulsus paradoxus is not
related to pulse rate or heart rate, and it is not a paradoxical rise in
systolic pressure. The normal variation of blood pressure during
breathing/respiration is a decline in blood pressure during
inhalation and an increase during exhalation.
Pulsus paradoxus is a sign that is indicative of several conditions,
including cardiac tamponade, chronic sleep apnea, croup, and
obstructive lung disease.
The paradox in pulsus paradoxus is that, on physical examination,
one can detect beats on cardiac auscultation during inspiration that
cannot be palpated at the radial pulse

62. Double Peaked Pulse
•Systolic percussion (LV) and tidal (peripheral) waves
(both in systole)
•Pulsus bisferiens
–Aortic regurgitation and / or aortic stenosis
•Bifid pulse (spike and dome)
–HOKMP
–PDA
–AV fistula

63. Pulsus parvus et tardus
•Pulse with slow and late peaks and less
fullness
•Frequently aortic stenosis
•Often with anacrotic notch
•The higher the severity of AS, the closer the
anachrotic notch to the top of the pulse.
A2
Anachrotic notch
Dicrotic notch

64. Dicrotic pulse
•Fast and strong pulse after S1 and 2nd peak
after S2 (in diastole)
•In bisferiens, both peaks should be in systole.
•Low CO + High SVR
•High CO + low SVR
S1
S2

65. Other pulse pathologies
•Pulse deficit
–Difference between radial pulse rate and peak heart rate counted by auscultation
–A.fibrillation with rapid ventricular response (not reflected on the radial pulse since
there is no effective CO in short diastole)
•Delay in radial-femoral pulse
–Normally the femoral palpates slightly earlier
–Femoral weak and delayed in aortic coarctation
–Takayasuda radial weaker and more delayed
•In supravalvular aortic stenosis, the right arm or carotid pulse is more
pronounced than the left (as the blood is thrown directly to the right side)
•Filiform pulse
–weak pulse in shock

66. The difference in blood pressure
between the two arms
•Normally, blood pressure of the right arm can be
higher by less than 10 mm Hg from the left.
•More difference or higher left than right
–Aorta narrowing, subclavian artery atherosclerosis-
embolism-arteritis,
–Extra 1. costa,
–scalenus anticus syndrome,
–thoracic outlet syndrome,
–subclavian stealing phenomenon,
–supravalvular aortic stenosis and
–aortic dissection

67. Specific conditions for aortic
regurgitation
•Hill sign
–Femoral systolic pressure approximately 40 mm Hg and above higher
than the radial (high volume and speed transmission of waves distal to
the aorta)
•Traube sign
•Pistol shot
–hearing the pulse on the femoral with a stethoscope in the form of a
powerful gun burst, both systolic and diastolic.
•Corrigan pulse (pulsus celer and altus)
•Water hammer pulse = splashing pulse
–Due to large amplitude upstroke and high CO-low resistance
•Duroziez sign
–Systolic and diastolic murmur over the femoral artery

68. Jugular venous pulse
•Preferably right jugular interna (directly related to the
right atrium)
•J V pressure:
•If the right atrium up to the Luis angle is more than 5
cm H2O + top of venous filling = 9 cm H2O, the JV
pressure has increased (1.36 cm H2O = 1 mm Hg)
•HJ reflux = 10-30 sec. Pressed to right upper quadrant.
An increase in vein pressure of 4 cm or more
compared to basal and if this value for more than 10
seconds is positive HJR

69. Jugular venous pressure (JVP)
•This evaluation tries to
evaluate the central venous
pressure and waveform.
•It is pathological if the
jugular vein fullness
(external jugular vein)
viewed at 45 degrees is
above 4 cm from the
sternal angle.
•Occurs when right
ventricular pressure
increases
***

70. Jugular vein pulsation
•While lying down, the
neck and body are raised
approximately 30
degrees. Right internal
jugular vein pulsation
occurs at the root of the
neck between the sternal
head of the
sternoclaidomastoid
muscle and the clavicle,
and should be separated
from arterial pulsation.

71. Jugular vein pulsation
•For the evaluation of venous
pulsation, an examination is
made at 30 degrees with the
neck muscles relaxed. To
differentiate in arterial
pulsation:
•Venous pressure pulsation is
double-crested
•Easy to inspect, difficult to
palpate
•Pressure applied to the
abdomen increases venous
pulsation

73. •High JVB;
•Decreased right ventricular
compliance (right ventricular failure
or infarction, pulmonary
hypertension, pulmonary stenosis)
with increased diastolic pressure.
•Obstruction in right ventricular inflow
(tricuspid stenosis, right atrial
myxoma, consrictive pericarditis,
pericardial tamponade),
•Tricuspid regurgitation,
•Vena cava superior obstruction (no
jugular venous pressure and
abdominojugular reflux negative)
•It is seen in cases of hypervolemia.
•Decreased JVB;
•Intravascular volume reduction

75. Jugular venous waveforms
•a = Atrial contraction (atrial systole)
•c = AV valve reflection during LV systole
•x descent = atrial relaxation during ventricular systole
•v = Increased positive pressure due to right atrium filling towards the end of LV
systole
•y descent = right ventricle filling in diastole with opening of the tricuspid valve
a
c
x
v
y

76. Pathologies associated with JV
waveforms
•There is no "a" wave in atrial fibrillation since
there is no atrium systole
•Giant “a” wave formed and reflected against
closed tricuspid valve in complete AV block
•Tricuspid stenosis, right vent. Hypertrophy,
pulmonary hypertension giant "a" and slow
"y" descent

77. Pathologies associated with JV
waveforms
•Significant "v" and rapid "y" descent in severe
TR or ASD
•Significant "x" and "y" descent in constrictive
pericarditis and restrictive CMP
•While there was a significant "x" descent in
cardiac tamponade, "y" descent was decreased

79. Hepatojugular reflux
•It is the occurrence of venous fullness by
pressing the hepatic area for 60 seconds or
exceeding the vanous filling> 4 cm. It is the
sign of hidden right heart failure

80. Kussmaul sign
•This is the paradoxical increase in JVP during
inspiration. JVP is normally reduced due to the drop
in intrathoracic pressure during inspiration and its
suction effect on the venous return. Therefore, the
Kussmaul sign is a true physiological paradox.
•Constrictive pericarditis
•Restrictive cardiomyopathy (sarcoidosis,
hemochromatosis, amyloidosis)
•Tricuspid stenosis,
•Vena cava superior syndrome.

81. Kussmaul sign
•Paradoxically, increased venous fullness of the
neck (JV pressure) during inspiration
–Constructive pericarditis
–Right ventricle MI
–Serious TR
–Pulmonary embolism
–Restrictive CMP

83. 83
Cardiovascular Physical Examination
4. Auscultation
•A silent environment, through the skin
•Stethoscope (Diaphragm / Bell)
•Auscultatory Sites

88. Cardiac Auscultation
•The diaphragm part of the The diaphragm part of the
stethoscope is used for high stethoscope is used for high
frequencies and the bell part is frequencies and the bell part is
used for low frequencies. Usually used for low frequencies. Usually
four positions are used routinely.four positions are used routinely.
•1- Left lateral decubitis,1- Left lateral decubitis,
•2- Supine (on the back)2- Supine (on the back)
•3- Sitting 3- Sitting
•4- leaning forward4- leaning forward
•Auscultation begins with the Auscultation begins with the
apex in the left lateral decubitus apex in the left lateral decubitus
position and all foci are rested.position and all foci are rested.

89. 89
Auscultatory Areas
1.Aortic area
2.Pulmonary area
3.Tricuspid area
4.Mitral area
5.Mesocardiac area
6.Supraclavicular area
7.Suprasternal area

90. 90
Auscultatory Areas
1.Aortic area: Right of the sternum, 2nd intercostal space (2nd ICA)
2.Pulmonary area: Left of the sternum, 2nd ICA
3.Tricuspid area: 4th ICA junction with the sternum
4.Mitral area: 5th ICA, midclavicular line (cardiac apex)
5.Mesocardiac area (Erb area): 3rd ICA junction with the sternum

91. 91
Auscultatory Areas
Listening areas are
not the anatomical
projections of the
heart valves, but the
points where the
blood flow through
the valves is best
heard.

92. 92
Auscultatory Areas

93. 93
Cardiac Auscultation
1.Heart Rate and Rhythm
2.Heart Sounds
1.Physiological sounds (S1, S2, rarely S3 and S4)
2.Pathological sounds (S3, S4, Galo Rhythms)
3.Additional sounds
4.Murmurs

94. 94
Heart Sounds
Normal Heart Sounds:
The sounds accompanying the work of the heart are called
heart sounds.
Auscultation → Listening the heart sounds with a
stethoscope over the auscultatory areas.
Phonocardiography → It is the recording of heart sounds
with an amplifier system.
Closure of heart valves plays an important role in the
formation of normal heart sounds.

95. 95
Differenciation of S1 and S2 from
each other
• Diastole> Systole
• S1> S2 at the apex;
• S2> S1 in 2
nd
IKA
• S1 coarser and muffled
• S2 is shorter, sharper and high frequency
• S1 just before pulse beat,
• S2 pulse is heard immediately after the beat.

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1. Heart Sound (S1)
•Occurs when A-V valves close
•It has two components (Mitral and Tricuspid)
•M1 is best heard in the mitral area, while T1 is
obtained more clearly in the tricuspid area
•Since the diastolic filling time will be longer at low
heart rate, the 1st sound gains a softer character.

97. 97
Increase in S1 Intensity
Mitral and tricuspid stenosis
The severe S1 in MD indicates that the mitral valve
is more flexible.
If S1 is weak or lost, it indicates that the mitral
valve is rigid-calcific.

98. 98
Decrease in S1 Intensity
Decrease in valve mobility:
MS and TS
Voice transmission problems:
Emphysema, obesity, pericardial
effusion, large chest, thick chest wall

99. 99
Split S1
•Normally, the first sound can sometimes be heard spiltted,
but it is very difficult to hear because the tricuspid closing
sound is very silent.
• Splitting becomes prominent in cases where the closure
of the tricuspid valve is delayed, such as complete right
bundle branch block, tricuspid stenosis, and large right-left
shunted ASD.
• In severe mitral stenosis, the advanced delay of mitral
valve closure disrupts the normal M1 T1, causing reverse
splitting (T1 M1).

100. 100
2. Heart Sound (S2)
•The mechanism of its occurrence is the closure of the
semilunar (aortic and pulmonary) valves.
• Components A2P2
•The best listening area are aortic and pulmonary artery
areas.

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Intensification of 2. Heart Sound
• The intensity of S2 is determined by
• Aortic and pulmonary artery pressures,
•the structure of the great vessels,
•the movement abilities of the aortic and pulmonary valves
• In systemic hypertension, aortic coarctation, ascending aortic aneurysm, the
aortic component (A2) of the second sound is heard hard (the second sound is
heard harder in the aortic area). There are two reasons for this hardening.
• The first is that the valves close more strongly due to the high pressure in
the aorta.
• The second reason is the overlap of the aortic and pulmonary components
of the second sound due to the prolonged left ventricular ejection.
Therefore, aortic second sound hardening can be easily noticed in all areas
including the apex of the heart.
• The most important factor that causes the second sound to be heard hard in
the pulmonary focus (hardening of the pulmonary component (P2) of the 2nd
sound) is pulmonary hypertension regardless of the cause.

102. 102
Decreased S2 Sound
•Arterial hypotension, MI, Heart failure, ShockArterial hypotension, MI, Heart failure, Shock
•Aortic stenosisAortic stenosis
•Pulmonary HTPulmonary HT
•Pulmonary stenosisPulmonary stenosis
•Deformities of the aorta and pulmonary valve.Deformities of the aorta and pulmonary valve.
•Murmurs covering S2Murmurs covering S2
•Obesity, Emphysema, pleural and pericardial effusion, PneumothoraxObesity, Emphysema, pleural and pericardial effusion, Pneumothorax

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Split S2
• Since the time between the closure of the aortic and pulmonary valves
is not long (10-20 msec.), The two are normally heard as a single sound,
but sometimes it is possible to hear the two components very close to
each other but separately.
• During deep inspiration, as the amount and duration of right
ventricular ejection increases with the increase in the amount of blood
returning to the right heart, the aortic and pulmonary components are
separated and the second sound is heard as a distinct pair, this is called
normal or physiological splitting.

104. 104
Split S2

105. 105
Narrow splitting of S2
Late A2 Early P
•LBBB · Pulmonary HT
•AR · Ageing
•PDA · RA tumor
•HT
•Ageing
•AS

106. 106
Widened Splitting of S2
•RBBB
•ASD, PR
•PS
•PE, RV failure
•Tamponade
•MR
•LA myxoma

107. 107
Fixed Splitting of S2
•A fixed split S2 is a rare finding
•It almost always indicates the presence of an ASD
•A fixed split S2 occurs when there is always a delay in the closure of
the pulmonic valve
•ASD
•During inspiration, as usual, there is an increase in venous return
to the right side of the heart and thus increased flow through the
PV — delaying its closure. The alteration in a person with an ASD
occurs during expiration. As the person expires, the pressure in
the right atrium decreases because there is less venous return.
The decreased pressure allows more blood to flow abnormally
through the ASD from the high pressured left atrium to the right
atrium, ultimately resulting again in increased flow through the
pulmonic valve — again, delaying its closure.

108. 108
Parodoxical Splitting of S2
•A paradoxical split S2 heart sound occurs when the
splitting is heard during expiration and disappears
during inspiration — opposite of the physiologic split
S2.
•A paradoxical split S2 occurs in any setting that delays
the closure of the aortic valve including
•severe aortic stenosis
•hypertrophic obstructive cardiomyopathy
•left bundle branch block.

109. 109
3. Heart Sound (S3)
•It can be physiological or pathological.
•Can be heard in 1 / 2- 1/3 of healthy individuals.
•It is heard at the beginning of diastole, during the rapid
filling of the heart.
•It consists of the vibration of the ventricle wall.

110. 110
3. Heart Sound (S3)
• It suggests left ventricular insufficiency or volume overload.
• The coexistence of the third sound and tachycardia is called the
ventricular gallop and is the most important listening finding of clinical
congestive heart failure.
• Similarly, the third sound heard in the foreground tricuspid focus is called
the right ventricular third sound, when it is associated with tachycardia, it is
called the right ventricular gallop and constitutes the most important
listening finding of right ventricular systolic insufficiency. The intensity of the
right ventricular gallon increases with deep inspiration.

111. 111
4. Heart Sound (S4)
•It can be heard in ¼ of healthy individuals.
•Heard very close to the 1st voice
•Occurs from vibration as blood passes to the ventricles
during atrial systole

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4. Heart Sound (S4)
• It occurs when blood thrown into the left ventricle actively with atrial
contraction at the end of diastole hits the ventricle wall and vibrates the
atrioventricular valves when they are still open.
• It is heard only in people with sinus rhythm because it is due to atrial
contraction.
• It is generally thought that the reason for the fourth sound, which is
comfortable, is a decrease in ventricular compliance (diastolic dysfunction).
• The presence of S4 with tachycardia is called atrial gallop and it is a sign of
left ventricular clinical diastolic insufficiency, it is common in conditions such
as hypertension, aortic stenosis, hypertrophic cardiomyopathy and coronary
artery disease.
• Right ventricular atrial galloes may also be encountered in conditions such
as pulmonary hypertension and pulmonary stenosis.

113. 113
Summation Gallop
• As a result of the shortening of the diastole due to
tachycardia, the atrial and ventricular gallops can
combine to create a single and strong sound, which
is called the summation gallop.

114. 114
Extra Heart Sounds
• Systolic Clicks
• Opening Snap
• Tumor Plop
• Pericardial Beat (knock)
• Frotman
• Prosthetic valve sound

115. 115
Systolic Click
* Additional sounds heard during systole are called systolic clicks.
Causes of midsystolic click:
Mitral valve prolapse
Pleuropericardial or pericardiodiaphragmatic adhesions
Pericarditis
Left pneumothorax
Mediastinal emphysema
Ejection click: Occurs immediately after the 1st sound and is heard in the
stenosis of the aortic or pulmonary valves and in the aortic root and
pulmonary artery enlargement. In these valve stenoses, the valve must
be mobile in order to form a click, no click is heard in calcific, advanced
fibrotic, adherent and immobile valves.
The greater the stenosis in the valve, the closer the click is to the first
sound.

116. 116
Opening Snap
Under normal conditions, no sound is heard when opening the mitral
and tricuspid valve.

The opening sound heard in mitral and tricuspid stenosis is the
vibration of the valve that is adhered to the commissures at the
beginning of the rapid filling phase.
In order for the opening sound to be heard, the valve must be
movable, just like ejection clicks. The opening sound disappears in
calcific, advanced fibrotic, adherent and immobile valves.
Apart from mitral stenosis, in cases where early diastolic flow velocity
is high (mitral insufficiency, PDA, VSD with wide left-right shunt), the
opening sound of the mitral valves may occur with sudden stretching.

117. 117
Opening Snap
Due to the opening of the AV valves at the beginning of diastole
High pitched / high frequency
Heard in MD and TD
A2 -OS = 70-110 msec (IVRT)
A2-OS determines the degree of mitral stenosis
A2-OS is reduced in severe MD
A2-OS decreases with tachycardia (diastole becomes shorter)
OS severity decreases at low CO

118. 118
Tumor Plop
The tumor sound heard in left atrial myxoma is similar to the opening
sound.
Echocardiographic examination showed that the sound was formed
when the tumor connected to the atrial septum stopped abruptly in
diastole as it protrudes rapidly from the mitral valve into the left
ventricle.

119. 119
Pericardial Knock
The pericardial knock heard in 70% of
cases of constrictive pericarditis is due
to the sudden stretching of the
thickened and reduced pericardium
during the rapid ventricular filling phase
and a sudden decrease in the ventricular
filling rate.

120. 120
Pericardial friction rub (frotman)
The inner and outer (visceral and parietal, respectively) layers of
pericardium are normally lubricated by a small amount of pericardial
fluid, but the
 inflammation of pericardium causes the walls to rub against
each other with audible friction

121. 121
Heart Murmurs
•Timing in the heart cycle (Systolic? Diastolic?)
• Duration (Midsystolic? Pansystolic? Early diastolic? Holodiastolic?)
• Intensity (1 / 6-6 / 6)
• Frequency (high frequency: treble / thin; low frequency: thick, bass)
• Quality (Hard, musical, absorbent ..)
• Where is it heard best (Apex? Aortic focus?)
• Propagation (carotid, axilla ..)
• Maneuvers and response to pharmacological agents

122. 122
Murmurs by Etiology
• Innocent murmur: The physiological murmur heard in healthy people
• Functional murmur: Due to increased circulation speed
• Organic murmur: due to heart lesion

123. 123
Murmurs by Localization
1. Systolic murmurs
-Midsystolic
-Pansystolic
-Early systolic
-Late systolic
2. Diastolic murmurs
-Early diastolic
-Mid diastolic
-Late diastolic
3.Systolo-diastolic murmurs
4. Continuous murmurs

124. 124
The severity of murmur
Systolic is 6 degrees.Systolic is 6 degrees.
1/6: hardly heard in a 1/6: hardly heard in a silentsilent environment. environment.
2/6: it is soft. But it is easily detected.2/6: it is soft. But it is easily detected.
3/6: It is evident. But it is not rude.3/6: It is evident. But it is not rude.
4/6: coarse and usually has trill.4/6: coarse and usually has trill.
5/6: very coarse.5/6: very coarse.
6/6: 6/6: CanCan be heard at close range without contact. be heard at close range without contact.
Diastolic is 4 degrees;Diastolic is 4 degrees;
1/4; hardly heard in a 1/4; hardly heard in a silentsilent environment environment
2/4: it is soft. But it is easily detected.2/4: it is soft. But it is easily detected.
3/4; It is distinct, easy to hear,3/4; It is distinct, easy to hear,
4/4: It is violent4/4: It is violent

125. 125
Systolic Murmurs
Mid-Systolic Ejection Murmurs:
Murmurs that occur with blood flow forward from a semilunar valve
during systole.
Properties:
In the form of Crescendo-decrescendo (increasing-decreasing in
intensity)
Ends before S2 of the side on murmur
Aggravated after long diastole
Example: Aortic stenosis, pulmonary stenosis, aortic coarctation,
increased cardiac output, children's innocent Still murmur

126. 126
Systolic Murmurs
Pansystolic Murmurs:
They start with S1 and last until S2
Soft, high frequency and blower
Their intensity does not change after a long diastole
Examples
Mitral regurgitation
Papillary muscle dysfunction
Chorda tendinea rupture
Rheumatic MR (pansystolic)
Mitral valve prolapse (mid-late systolic, crescendo to S2)
Tricuspid regurgitation
Ventricular septal defect

127. 127
Systolic Murmurs
Late-systolic Murmurs:
Mild to moderate mitral regurgitation
Papillary muscle dysfunction (MY)
Hypertrophic obstructive cardiomyopathy
Aortic coarctation
Mitral valve prolapse

128. 128
Diastolic Murmurs
•Early DiastolicEarly Diastolic
•ARAR
•PRPR
•Graham steelGraham steel
•Carey-CoombsCarey-Coombs
•Mid-diastolicMid-diastolic
•MSMS
•TSTS
•MyxomaMyxoma
•High-flow: MR, VSD, PDA, ASDHigh-flow: MR, VSD, PDA, ASD
•Late diastolicLate diastolic
•MSMS
•Austin-FlintAustin-Flint

129. 129
Systalo-diastolic Murmurs
• AS + AR
• MS + MR
• VSD + AR

130. 130
Continuous Murmurs
•Patent duktus arteriosus (left 2nd ICS)
• Aorto-pulmonary septal defect (left 3rd-4th ICS)
• Aortic corctation
• Pregnancy
• Postpartum
• Atria or right ventricular coronary artery fistula
• Valsalva sinus aneurysm rupture
• Pulmonary / peripheral AV fistula

131. 131
A good physical examination is more valuable than any expensive and
technological diagnostic tools.