Download cardiovascular examination

Common Approach to
Cardiovascular Diseases /
Physical Examination
Prof. Dr. Muzaffer Değertekin
[email protected]
Yeditepe Univ. Hospital – 3rd Floor
March 2015
Cardiology
Physical Examination
Coronary Artery Disease
ECG
Heart Failure
Heart Valve Disease
Acute Coronary Syndromes
Restrictive and Hypertrophic Cardiomyopathy
Cardiac Rhythm Problems
EXAMINATION of the
CARDIOVASCULAR SYSTEM
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General inspection
Specific inspection
Pulse
Carotid
Neck veins
Praecordium
Auscultation
Lung bases,liver, ankles
Veins and arteries in the legs
GENERAL INSPECTION
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General build and appearence
Colour
Respiration (abnormal breathing
pattern, shortness of breath)
Signs of distress and response
Conscious level
SPECIFIC INSPECTION
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Cyanosis
– Central: mucous membranes-tongue
– Peripheral: extremities
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Clubbing
Anemia
Edema
Peripheral perfusion
Body habitus
Specific signs of cardiac pathologies: IE stigmata,
arcus senilis, xanthome and xanthelasma
CYANOSIS and CLUBBING
Signs of atherosclerosis
Xanthelesma
Arcus juvenilis
Sign of premature atherosclerosis
xanthoma
IE/specific signs
Body habitus: Marfan
syndrome, thorax
abnormalities
Apical Impulse:
Visualization
to assess ventricular size/thickness
Normally distinct and located at 4ICS at/inside the midclavicular line
Apical Impulse
(abnormal):
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Hyperdynamic impulse in normal
location: think increased cardiac
output or LVH
Hyperdynamic and
downward/leftwardly displaced: think
LVE
Indistinct impulse associated with RVH
Precordial heave is seen with RVE
Thrills:
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Palpation of a loud murmur
Found in the precordial, suprasternal,
or carotid artery area
If low intensity murmur, probably just
a pulsation and NOT a thrill
Juguler venous pulse
Patient position for JVP
assessment
JVP measurement
HJR and Kussmaul’s sign
Jugular Venous Pressure
Waveform
The PULSE
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Rate
– Normal sinus 60-100bpm
– Sinus bradycardia <60 bpm
– Sinus tachycardia >100 bpm
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Regularity
– Sinus arrhytmia: varies with respiration
– Intermittant irregularity: ectopic beats
– Continously irregular: atrial fibrillation
Pulse volume and contour
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Palpation of large vessels
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Forearm, brachial, carotid, femoral
Volume: normal/increased/decreased
Pulse pattern:
•Slow rising+/ brachial-radial delay (AS)
•Collapsing (waterhammer) pulse (AR)
•Bifid-Bisferiens (AS+AR, IHSS)
•Pulsus paradoxus (Pericardial tamponade,
COPD)
•Pulsus alternans (LV dysfunction)
Nabız Tipleri / Pulsation Types
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Pulsus Tardus (Yavaş Yükselen)
Pulsus Parvus (Küçük Amplitüdlü)
Dolgun Nabız (Nabız Basıncı Artmış)
Corrigan Nabız
Pulsus Altus ve Celer
Pulsus Bisferiens
Pulsus Alternans
Pulsus Bigeminus
Pulsus Paradoksus
Dikrotik Nabız
Auscultation
Heart Sounds
Timing of Heart Sounds
S1 (cont.):
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If split heard better at the apex, may
actually be S4 or ejection click
Tends to be more low-pitched and
long as compared to S2
Differentiate S1 from S2 by palpating
carotid pulse:
 S1 comes before and S2 comes after
carotid upstroke
Decreased S1:
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Slowed ventricular
ejection
rate/volume
Mitral insufficiency
Increased chest
wall thickness
Pericardial effusion
Hypothyroidism
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Cardiomyopathy
LBBB
Shock
Aortic insufficiency
First degree AV
block
Other Abnormal S1
(cont.):
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Increased S1:
 Increased cardiac output
 Increased A-V valve flow velocity (mitral
stenosis)
S2:
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From closure vibrations of aortic and
pulmonary valves
Divided into A2 and P2 (aortic and
pulmonary closure sounds)
Best heard at LMSB/2LICS
Higher pitched than S1/better heard
with diaphragm
S2 splitting (normal):
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Normally split due to different
impedance of systemic and pulmonary
vascular beds
Audible split with > 20 msec
difference
Split in 2/3 of newborns by 16 hrs. of
age, 80% by 48 hours
Harder to discern in heart rates > 100
bpm
S2 splitting (normal,
cont.):
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Respiratory variation causes  splitting
on inspiration:  pulmonary vascular
resistance
When supine, slight splitting can occur
in expiration
When upright, S2 usually becomes
single with expiration
S2 splitting (abnormal,
cont.):
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Fixed splitting
 ASD
S2 splitting (abnormal,
cont.):
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Wide /mobile
splitting
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Mild PS
RVOTO
Large VSD or PDA
Idiopathic PA
dilation
 Severe MR
 RBBB
 PVC’s
S2 splitting (abnormal,
cont.):
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Reversed splitting
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LBBB
WPW
Paced beats
PVC’s
AS
PDA
LV failure
Extra heart sounds
S3 (gallop):
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Usually physiologic
Low pitched sound, occurs with rapid
filling of ventricles in early diastole
Due to sudden intrinsic limitation of
longitudinal expansion of ventricular
wall
S3 (cont.):
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Best heard with patient supine or in
left lateral decubitus
Increased by exercise, abdominal
pressure, or lifting legs
LV S3 heard at apex and RV S3 heard
at LLSB
S3 (abnormal):
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Seen in HF, severe MR--disappears
after treatment
S4 (gallop):
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Nearly always pathologic
Can be normal in elderly or athletes
Low pitched sound in late diastole
Due to elevated LVEDP (poor
compliance) causing vibrations in stiff
ventricular myocardium as it fills
S4 (cont.):
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Better heard at the apex or LLSB in
the supine or left lateral decubitus
position
Occurs separate from S3 or as
summation gallop (single intense
diastolic sound) with S3
S4 Associations:
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CHF!!!
HCM
severe systemic HTN
pulmonary HTN
Ebstein’s anomaly
myocarditis
S4 Associations (cont.):
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Tricuspid atresia
TAPVR
CoA
AS
Kawasaki’s disease
Ejection clicks
Timing of Heart Sounds
Cardiac murmurs
Basic Pathophysiology
Systolic
Diastolic
Describing a heart murmur
1. Timing
– murmurs are longer than heart sounds
– HS can distinguished by simultaneous palpation of
the carotid arterial pulse
– systolic, diastolic, continuous
2. Shape
– crescendo (grows louder), decrescendo, crescendodecrescendo, plateau
3. Location of maximum intensity
– is determined by the site where the murmur originates
– e.g. A, P, T, M listening areas
Describing a heart murmur
con’t:
4. Radiation
– reflects the intensity of the murmur and the direction
of blood flow
5. Intensity
– graded on a 6 point scale
Grade 1 = very faint
 Grade 2 = quiet but heard immediately
 Grade 3 = moderately loud
 Grade 4 = loud
 Grade 5 = heard with stethoscope partly off the chest
 Grade 6 = no stethoscope needed
*Note: Thrills are assoc. with murmurs of grades 4 - 6
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Describing a heart murmur
con’t:
6. Pitch
– high, medium, low
7. Quality
– blowing, harsh, rumbling, and musical
8. Others:
i. Variation with respiration
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Right sided murmurs change more than left sided
ii. Variation with position of the patient
iii. Variation with special maneuvers
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Valsalva/Standing => Murmurs decrease in length and intensity
EXCEPT: Hypertrophic cardiomyopathy and Mitral valve
prolapse
Systolic Murmurs
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Derived from increased turbulence associated
with:
1. Increased flow across normal SL valve or into a
dilated great vessel
2. Flow across an abnormal SL valve or narrowed
ventricular outflow tract - e.g. aortic stenosis
3. Flow across an incompetent AV valve - e.g. mitral
regurg.
4. Flow across the interventricular septum
Systolic Murmurs
Early Systolic murmurs
1. Acute severe mitral regurgitation
– decrescendo murmur
– best heard at apical impulse
– Caused by:
i. Papillary muscle rupture
ii. Infective endocarditis
iii. Rupture of the chordae tendineae
iv. Blunt chest wall trauma
2. Congenital, small muscular septal defect
3. Tricuspid regurg. with normal PA pressures
Midsystolic (ejection)
murmurs
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Are the most common kind of heart murmur
Are usually crescendo-decrescendo
They may be:
1. Innocent
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common in children and young adults
2. Physiologic
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can be detected in hyperdynamic states
e.g. anemia, pregnancy, fever, and hyperthyroidism
3. Pathologic
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are secondary to structural CV abnormalities
e.g. Aortic stenosis, Hypertrophic cardiomyopathy, Pulmonic
stenosis
Pansystolic (Holosystolic)
Murmurs
Are pathologic
 Murmur begins immediately with S1 and continues up to
S2
1. Mitral valve regurgitation
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– Loudest at the left ventricular apex
– Radiation reflects the direction of the regurgitant jet
i. To the base of the heart = anterosuperior jet (flail posterior
leaflet)
ii. To the axilla and back = posterior jet (flail anterior leaflet
– Also usually associated with a systolic thrill, a soft S3, and a short
diastolic rumbling (best heard in left lateral decubitus
2. Tricuspid valve regurgitation
3. Ventricular septal defect
Diastolic Murmurs
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Almost always indicate heart disease
Two basic types:
1. Early decrescendo diastolic murmurs
– signify regurgitant flow through an imcompetent semilunar
valve
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e.g. aortic regurgitation
2. Rumbling diastolic murmurs in mid- or late diastole
– suggest stenosis of an AV valve
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e.g. mitral stenosis
Diastolic Murmurs
Continuous Murmurs
Begin in systole, peak near s2, and continue into all or
part of diastole.
1. Cervical venous hum
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– Audible in kids; can be abolished by compression over the IJV
2. Mammary souffle
– Represents augmented arterial flow through engorged breasts
– Becomes audible during late 3rd trimester and lactation
3. Patent Ductus Arteriosus
– Has a harsh, machinery-like quality
4. Pericardial friction rub
– Has scratchy, scraping quality
Back to the Basics
1. When does it occur - systole or diastole
2. Where is it loudest - A, P, T, M
I. Systolic Murmurs:
1. Aortic stenosis - ejection type
2. Mitral regurgitation - holosystolic
3. Mitral valve prolapse - late systole
II. Diastolic Murmurs:
1. Aortic regurgitation - early diastole
2. Mitral stenosis - mid to late diastole
SUMMARY
A. Presystolic murmur
– Mitral/Tricuspid stenosis
B. Mitral/Tricuspid regurg.
C. Aortic ejection murmur
D. Pulmonic stenosis (spilling
through S20
E. Aortic/Pulm. diastolic
murmur
F. Mitral stenosis w/ Opening
snap
G. Mid-diastolic inflow murmur
H. Continuous murmur of PDA
Summary
Innocent murmurs
Characteristics of
Pathologic Murmurs
Ankle-brachial index
(ABI)